Studies of IFNGR1 turnover have revealed that interfering with palmitoylation, the covalent attachment of fatty acids to cysteine and less frequently to serine and threonine residues of proteins, can restore IFNγ signaling in CRC, and thereby enhance T cell activity and sensitize tumors to immunotherapy[63].These preclinical studies suggest that stabilizing IFNGR1 by inhibiting its palmitoylation may be a viable strategy for overcoming resistance to ICB in CRC. The gene discussed is IFNGR1; the disease is colorectal carcinoma.