KRAS mutations in lung cancer also increase the expression of Acyl-coenzyme A synthetase long chain family member 3 (ACSL3) to reprogram lipid metabolism, promote Monounsaturated fatty acids-phospholipids (MUFA-PL) biosynthesis and ferroptosis resistance, and facilitate lung cancer progression (Friedmann Angeli et al., 2014; Padanad et al., 2016). This evidence concerns the gene ACSL3 and lung carcinoma.