Current understanding suggests that gene mutations in the hypothalamus, particularly leptin signaling, can contribute to NAFLD and obesity [15]; gut permeability differences can result in the leak of pro-inflammatory signals that contribute to NAFLD [16,17]; resistance to insulin in adipose tissue can result in the redistribution of fat to other organs, including the liver [18]; and the release of adipokines and cytokines among others contributing to NAFLD [19]. The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.