Ample clinical data support a role for IL6 in acute myeloid leukemia (AML) chemoresistance, but underlying mechanisms are poorly defined. In their study on page 1366, Hou and colleagues used primary AML samples, cell lines, and a mouse model to show that IL6 directly fortifies oxidative phosphorylation by elevating mitofusin 1 (MFN1) expression and promoting mitochondrial fusion in AML cells. shRNA-mediated MFN1 ablation was sufficient to disrupt IL6-mediated chemoresistance in vitro. Accordingly, antibody-mediated IL6 depletion reduced MFN1 protein expression and increased AML cell sensitivity to standard chemotherapy in vivo. The cover image depicts creative renderings of AML cell immunofluorescent confocal micrographs, where translocase of outer mitochondrial membrane 20 (TOMM20)-probed mitochondria fluoresce red and DAPI-stained nuclei fluoresce blue.