TECR (trans-2,3-enoyl-CoA reductase) is an endoplasmic reticulum-bound enzyme that catalyzes the final reduction step in the elongation of very-long-chain fatty acids (VLCFAs), adding two-carbon units per cycle to produce fatty acids longer than 16 carbons 1. This process is essential for synthesis of VLCFAs that serve as precursors for membrane lipids and lipid mediators. TECR also participates in sphingolipid metabolism, catalyzing saturation of trans-2-hexadecenoyl-CoA to palmitoyl-CoA in the sphingosine 1-phosphate pathway. Biallelic loss-of-function variants in TECR cause autosomal recessive non-syndromic intellectual disability, with cases of Hutterite ancestry expanding the known phenotype to include dolicocephaly and corpus callosum dysgenesis 2. Beyond inherited metabolic disease, recent evidence indicates TECR functions in cancer cell biology: the drug candidate tegavivint triggers a TECR-dependent, non-apoptotic cell death mechanism distinct from ferroptosis, necroptosis, and pyroptosis, occurring through TECR-mediated palmitate synthesis 3. Upregulation of TECR is associated with colorectal cancer progression in obese individuals, where it participates in unsaturated fatty acid biosynthesis pathways that cross-talk with arachidonic acid and PPAR signaling 4. Tegavivint's mechanism offers a potential therapeutic avenue currently being evaluated in human clinical trials.