While in many tributes these modes exist in an uneasy disjunction, others employ creative reflection to suggest new modes of knowledge and identity which may inform ethical practice. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.Pre-exposure prophylaxis (PrEP) (Truvada) is a medication which if taken correctly is almost entirely effective in preventing HIV infection. In regions and countries where it has been widely taken up, HIV seroconversion rates have significantly decreased. Alongside testing and treatment, it offers the very real prospect of ending HIV infections. However, in England, commissioning it has (and still is) a controversial process, where NHS England has repeatedly raised supposed ‘uncertainties’, first legal and then scientific. The same has not happened in Scotland, where PrEP was commissioned to anyone who needed it in April 2017. This article presents a close reading of the IMPACT trial protocol, which we conclude cannot answer the questions it sets out to answer. We then suggest that the uncertainties the trial claims to address are in fact a tool of power which is deployed to strategically ration healthcare; introduce uncertainty about commissioning PrEP; and shift the boundary between individual responsibilities and state responsibilities for public health and HIV prevention. We conclude that all the above constitute an unethical use of clinical trial rhetoric, systematically discriminate against minority and vulnerable groups, and ration healthcare for those who most need it. As such, we call on all academics, clinicians and activists to resist further unethical misuses of clinical trial rhetoric. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.A significant therapeutic challenge for cancer patients is resistance to chemotherapies such as taxanes. Overexpression of LIN9, a transcriptional regulator of cell cycle progression, occurs in 65% of patients with triple negative breast cancer (TNBC), a disease commonly treated with these drugs. Here we report that LIN9 is further elevated with acquisition of taxane resistance. Inhibiting LIN9 genetically or by suppressing its expression with a global BET inhibitor restored taxane sensitivity by inducing mitotic progression errors and apoptosis. While sustained LIN9 is necessary to maintain taxane resistance, there are no inhibitors that directly repress its function. Hence, we sought to discover a druggable downstream transcriptional target of LIN9. Using a computational approach, we identified NIMA-related Kinase 2 (NEK2), a regulator of centrosome separation that is also elevated in taxane-resistant cells. High expression of NEK2 was predictive of low survival rates in patients who had residual disease following treatment with taxanes plus an anthracycline, suggesting a role for this kinase in modulating taxane sensitivity. Like LIN9, genetic or pharmacologic blockade of NEK2 activity in the presence of paclitaxel synergistically induced mitotic abnormalities in nearly 100% of cells and completely restored sensitivity to paclitaxel, in vitro. In addition, suppressing NEK2 activity with two distinct small molecules potentiated taxane response in multiple in vivo models of TNBC, including a patient-derived xenograft, without inducing toxicity. These data demonstrate that the LIN9/NEK2 pathway is a therapeutically targetable mediator of taxane resistance that can be leveraged to improve response to this core chemotherapy. Copyright ©2020, American Association for Cancer Research.Adipocytes are critical for ovarian cancer (OvCa) cells to home to the omentum, but the metabolic changes initiated by this interaction are unknown. To this end, we carried out unbiased mass spectrometry-based metabolomic and proteomic profiling of cancer cells co-cultured with primary human omental adipocytes. Cancer cells underwent significant proteo-metabolomic alteration(s), typified by changes in the lipidome with corresponding upregulation of lipid metabolism proteins. FABP4, a lipid chaperone protein, was identified as the critical regulator of lipid responses in OvCa cells co-cultured with adipocytes. Subsequently, knockdown of FABP4 resulted in increased 5-hydroxymethylcytosine levels in the DNA, downregulation of gene signatures associated with OvCa metastasis and reduced clonogenic cancer cell survival. In addition, CRISPR-mediated knockout of FABP4 in high-grade serous OvCa cells reduced metastatic tumor burden in mice. Consequently, a small molecule inhibitor of FABP4 (BMS309403) not only significantly reduced tumor burden in a syngeneic orthotopic mouse model but also increased the sensitivity of cancer cells towards carboplatin both in vitro and in vivo. Taken together, these results show that targeting FABP4 in OvCa cells can inhibit their ability to adapt and colonize lipid-rich tumor microenvironments, providing an opportunity for specific metabolic targeting of OvCa metastasis. All trans-Retinal Copyright ©2020, American Association for Cancer Research.Biodiversity is declining at unprecedented rates worldwide. Yet cascading effects of biodiversity loss on other taxa are largely unknown because baseline data are often unavailable. We document the collapse of a Neotropical snake community after the invasive fungal pathogen Batrachochytrium dendrobatidis caused a chytridiomycosis epizootic leading to the catastrophic loss of amphibians, a food source for snakes. After mass mortality of amphibians, the snake community contained fewer species and was more homogeneous across the study site, with several species in poorer body condition, despite no other systematic changes in the environment. The demise of the snake community after amphibian loss demonstrates the repercussive and often unnoticed consequences of the biodiversity crisis and calls attention to the invisible declines of rare and data-deficient species. Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.