Increased uptake of plasma FFAs derived from lipolysis in adipose tissue significantly contributes to NAFLD development, as studies of liver-specific knockout of FATP2 and FATP5 have established decreased FA uptake and hepatic steatosis [85,86], whereas liver-specific overexpression of fatty acid translocase (FAT/CD36) aggravates the condition [86]. The gene discussed is CD36; the disease is metabolic dysfunction-associated steatotic liver disease.