DHCR7 (7-dehydrocholesterol reductase) catalyzes the final step of cholesterol biosynthesis, converting 7-dehydrocholesterol (7-DHC) to cholesterol 1. It functions as a component of the microsomal antiestrogen binding site complex at the ER membrane, contributing to cholesterol-5,6-epoxide hydrolase activity 2. Beyond cholesterol metabolism, DHCR7 has emerged as a key regulator of ferroptosis—a form of iron-dependent cell death. DHCR7 inhibition increases 7-DHC accumulation, which acts as a potent antioxidant by trapping radicals and shielding lipids from phospholipid peroxidation, thereby suppressing ferroptosis 34. Consequently, DHCR7 functions paradoxically as a pro-ferroptotic gene whose inhibition prevents ferroptosis-related liver injury 4. DHCR7 also regulates innate immune responses; its inhibition promotes IRF3-mediated type I interferon production and enhances viral clearance 5. In cancer contexts, DHCR7 upregulation promotes metastasis through cholesterol-dependent signaling mechanisms including PI3K/AKT activation and VEGF-C secretion 6. Loss-of-function mutations in DHCR7 cause Smith-Lemli-Opitz syndrome, characterized by severe developmental abnormalities and cholesterol deficiency 1. Pharmacological DHCR7 inhibition shows therapeutic potential for cancer, metabolic liver disease, ischemia-reperfusion injury, and viral infections.