However, the results in vitro showed that miR-667-5p significantly raised the p62 protein levels and TG and TC contents, which was in line with those obtained after SIRT1 knockdown, further suggesting that miR-667-5p mimic or knockdown of SIRT1 might promote NAFLD by inhibiting autophagic flux. Here, SIRT1 is linked to metabolic dysfunction-associated steatotic liver disease.