For example, it was found that DHHC2 was abnormally upregulated in tyrosine kinase inhibitor-resistant clear cell renal cell carcinoma tissues and cells, and the upregulation of DHHC2 increased the S-palmitoylation of AGK, which promoted the translocation of AGK to the PM for further activation of the PI3K/Akt/mTOR pathway, finally leading to TKI resistance.119 In addition, in colorectal cancer, the accumulation of palmitic acid caused by ACOX1 depletion contributes to the enhanced S-palmitoylation of β-catenin. The gene discussed is AGK; the disease is colorectal cancer.