The latest study found that deletion of selenoprotein M (SELENOM) exacerbated HFD‐induced the presence of steatosis, inflammation, and fibrosis in the liver in obese mice, an increase in fatty acid oxidation and oxidative stress in the liver is associated with this condition; over‐expression of SELENOM activated Parkin‐mediated mitophagy through the AMPKα1‐MFN2 pathway, which cleared HFD‐damaged mitochondria.52 This evidence concerns the gene SELENOM and steatosis.