For instance, continuously increased leptin and pro-inflammatory mediators (cytokines and chemokines), for example, tumor necrosis factor alpha (TNF-α), nuclear factor kappa β (NF-κβ) and chemoattractant protein-1 (MCP-1), and reduced adiponectin and anti-inflammatory markers such as interleukin-10 are likely to promote NASH progression and initiate fibrosis formation [23,24,25,26]. This evidence concerns the gene ADIPOQ and metabolic dysfunction-associated steatohepatitis.