PA induces insulin resistance and pancreatic β-cells dysfunction via three mechanisms (27): (1) Increased internalization of palmitic acid results in lipotoxicity (28); (2) The excess of PA results in the endoplasmic reticulum and mitochondria dysfunction (29, 30); (3) PA can activate toll-like receptor (TLR)-4 and high-fat diets activate the IKKβ–NF-κB pathway, leading to an inflammatory environment (31, 32). The gene discussed is IKBKB; the disease is Insulin resistance.