In summary, by using the RRA method we have successfully provided deeper insight to the comprehensive molecular changes in NAFLD pathogenesis, and identified several potential candidate therapeutic targets, including ENO3, CYP7A1, P4HA1, CYP1A1, IGFBP2, SOCS2, FMO1, PEG10, SHBG, and MAMDC4. This evidence concerns the gene SOCS2 and metabolic dysfunction-associated steatotic liver disease.