MASLD, particularly when it progresses to MASH, leads to the intrahepatic production and systemic release of pro-inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and C-reactive protein (CRP) [59,82]. This evidence concerns the gene TNF and metabolic dysfunction-associated steatohepatitis.