Metabolically, the lipid-rich microenvironment in NAFLD activated de novo palmitate biosynthesis in hepatic metastatic CRC cells by upregulating fatty acid synthase (FASN) expression and boosting endogenous palmitate production to promote EGFR palmitoylation for its PM localization and evasion from lysosomal degradation. This evidence concerns the gene EGFR and metabolic dysfunction-associated steatotic liver disease.