One of the new findings to emerge is that omental and mesenteric fat storage cells constitute a major endocrine influence on the liver and that the imbalance of their adipokines (e.g. leptin, adiponectin, visfatin, apelin and resistin) induces hepatic fat deposition, insulin resistance (IR) and progression to NASH [22,25]. This evidence concerns the gene LEP and metabolic dysfunction-associated steatohepatitis.