Concurrently, UTX deficiency leads to stabilization of phenylalanine hydroxylase and increased tyrosine secretion, which promotes myeloid-derived suppressor cell (MDSC)-mediated immunosuppression and metastasis through STAT5 activation, exemplifying the crosstalk between metabolic and epigenetic regulation in CRC progression [75].Moreover, SETDB1-mediated H3K9 methylation activates Akt signaling preferentially in KRAS-mutant CRC, contributing to tumorigenicity and chemoresistance, positioning SETDB1 as a potential therapeutic target [76]. Here, KRAS is linked to colorectal carcinoma.