In summary, as shown in Fig. 8h, our findings reveal a novel mechanism by which uc.372 drives hepatic steatosis by repressing the maturation of miR-195/miR-4668, thus relieving the suppression of target genes, including ACC, FAS, SCD1, and CD36. We also propose that uc.372 inhibitors might be potential therapeutic agents for NAFLD. The gene discussed is FAS; the disease is Hepatic steatosis.