Given the proinflammatory roles of lipoxygenase and cyclooxygenase signaling, this is a plausible mechanism through which KRAS-induced lipid metabolism may augment tumor immunogenicity in our cohort, which may be ameliorated upon STK11 mutation and the presumptive shift of tumor cell metabolism away from lipolysis and toward anaerobic glycolysis. The gene discussed is STK11; the disease is neoplasm.