Furthermore, anti-PCSK9 therapy has a promising potential of reducing autophagy by inhibiting mammalian rapamycin targeting protein (mTOR) via increasing protein kinase B. However, the role of anti-PCSK9 therapy remains controversial in treating liver fibrosis, liver inflammation, and nonalcoholic steatohepatitis (NASH) [13–15]. This evidence concerns the gene PCSK9 and metabolic dysfunction-associated steatohepatitis.