FAS and metabolic dysfunction-associated steatotic liver disease: 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.