MTOR and colonic neoplasm: It has been reported that inhibition of Lyn can block the endocytosis of CD36 and thus inhibit the intake of fatty acids.[62] In addition, Lyn can regulate the metabolic reprogramming of free fatty acids to promote inflammation in steatohepatitis tissues.[63] Hippocalcin‐like protein 1 inhibits liver lipid metabolism by directly targeting RUVBL1‐mTOR signal transduction to inhibit tumorigenicity.[64] Metabolomics revealed that AA metabolism was inhibited in colon cancer cells after Lyn/RUVBL1 was knocked down.