However, current studies have revealed that the substrate required for ABCA1-mediated (i.e., ApoA-I and preβ1-HDL) CEC was significantly reduced in patients with NAFLD, which suggests that ApoA-I and preβ1-HDL are the cause of the deterioration observed in HDL CEC (57). This evidence concerns the gene APOA1 and metabolic dysfunction-associated steatotic liver disease.