In conclusion, our findings showed that the substrate for ABCA1-mediated CEC (i.e. ApoA-I and preβ1-HDL) was significantly suppressed in NAFLD patients indicating that ApoA-I and preβ1-HDL could be the cause of the impairment observed in HDL CECs. This evidence concerns the gene ABCA1 and metabolic dysfunction-associated steatotic liver disease.