FADS1 (fatty acid desaturase 1) is a membrane-associated oxidoreductase that catalyzes the conversion of linoleic acid to arachidonic acid (AA), serving as a rate-limiting enzyme in polyunsaturated fatty acid (PUFA) biosynthesis 1. The enzyme exhibits acyl-CoA desaturase activity and functions primarily in the endoplasmic reticulum and mitochondrial membranes to regulate unsaturated fatty acid metabolism and lipid homeostasis 2. Mechanistically, FADS1 upregulation drives AA synthesis, which subsequently metabolizes to pro-inflammatory prostaglandin E2 (PGE2) via downstream signaling cascades 13. In the tumor microenvironment, FADS1 expression in cancer-associated cells promotes immunosuppression by enhancing PGE2 signaling in tumor-associated neutrophils, preventing anti-tumor interferon responses 3. Clinically, FADS1 dysregulation is implicated in cancer progression and ferroptosis sensitivity. FADS1-high triple-negative breast cancer exhibits enhanced susceptibility to ferroptosis-inducing agents through PUFA accumulation, while genetic or pharmacological FADS1 inhibition confers resistance 4. Similarly, in gastric cancer, silencing of FADS1 through DNA methylation reduces ferroptosis sensitivity, whereas restoration of AA synthesis restores ferroptosis vulnerability 5. Common FADS1 polymorphisms (rs174549, rs174546, rs174537) significantly alter PUFA and AA levels in serum lipids and modify cardiovascular and metabolic disease risk across ethnic populations 62, suggesting potential for precision nutrition strategies.