In this study, we suggested a novel mechanism by which uc.372 drives hepatic steatosis through inhibition of miR-195/miR-4668 maturation to relieve miR-195/miR-4668-mediated suppression of functional target gene related to lipid synthesis, including acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1), and genes related to lipid uptake such as CD36, leading to hepatic lipid accumulation. The gene discussed is CD36; the disease is fatty liver disease.