Down‐regulation of ACSL5 or PI3K/ERK inhibition resulted in the loss of metabolism sensitivity to lysoPC in lung cancer cells, through remodelling patterns and efficiency of lipid metabolism, influencing mitochondrial function and respiration or leading to TAG accumulations by increasing TAG synthesis or delaying TAG absorption, similar to the findings based on the ablation of ACSL5 in the in vivo model and on the regulation of ACSL5 in the TAG synthesis.64, 65. The gene discussed is ACSL5; the disease is lung cancer.