For example, KRAS and LKB1 mutant non-small cell lung cancer (NSCLC) cells synthesize pyrimidines by upregulating CPS1 to provide raw materials for proliferation (9); lipid metabolism reprogramming in hepatocellular carcinoma alters cell membrane fluidity and mediates migration activity (12); when chemotherapy-sensitive lung adenocarcinoma cells are transformed into drug-tolerant persister cells, this transformation is closely related to PINK1-mediated mitophagy, enhanced OXPHOS, and cellular redox imbalance (5). The gene discussed is PINK1; the disease is non-small cell lung carcinoma.