In the development of obesity-related NAFLD, there is a crosstalk between the liver and the adipose tissue, the latter being an endocrine and immune organ able to release in the bloodstream a variety of pro-inflammatory chemokines and adipokines, e.g., leptin, IL-6 and TNF-α, that orchestrate NAFLD development [14]. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.