TECR (trans-2,3-enoyl-CoA reductase) is an endoplasmic reticulum-bound enzyme catalyzing the final reduction step in long-chain fatty acid elongation 1. It reduces trans-2,3-enoyl-CoA intermediates to acyl-CoA substrates, enabling addition of 2-carbon units per cycle to produce very-long-chain fatty acids (VLCFAs) with diverse biological functions 1. TECR also participates in sphingosine 1-phosphate metabolism, converting trans-2-hexadecenoyl-CoA to palmitoyl-CoA 2. The enzyme functions within a membrane-bound complex involving HACD1/2 and fatty acid elongases, with critical catalytic residues including Y248 that provides protons to substrates 3. Beyond canonical lipid synthesis, TECR promotes novel, TECR-dependent nonapoptotic cancer cell death distinct from ferroptosis, necroptosis, and pyroptosis, with tegavivint (a clinical drug candidate) activating this mechanism via palmitate synthesis 4. Pathologically, homozygous TECR variants cause intellectual developmental disorder with expanded phenotypes including dolicocephaly and corpus callosum dysgenesis, particularly identified in Hutterite populations 5. TECR expression is also dysregulated in Kaposi's sarcoma and esophageal cancer stem cells 67, and epigenetic regulation of TECR correlates with circulating adiponectin levels in lipid metabolism 8.