Indeed, the overexpression through adenoviral injection of KLF2 induced marked hepatic TGs accumulation and FFA uptake, in parallel to an elevation of Cd36 mRNA and protein levels in mice; whereas hepatocyte-specific Klf2 deficiency improved NAFLD features in ob/ob mice, including the normalisation of CD36 levels102. The gene discussed is CD36; the disease is metabolic dysfunction-associated steatotic liver disease.