One possible mechanism explaining the increased risk of colorectal neoplasia in NAFLD patients with advanced fibrosis is a pro-inflammatory and insulin-resistant condition that elevates serum insulin and insulin-like growth factor-1 (IGF-1), which in turn may promote growth and anti-apoptosis of colorectal neoplasia [25,35,52]. The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.