In view of these evidences, although androgens and androgen receptor (AR) contribute to the sex-based hepatic phenotype in a direct or indirect fashion, by acting on GH dependent pathways (200, 215, 233, 243) and by regulating the accessibility of DNA to several transcription factors through chromatin remodeling (244, 245), this review will focus in particular on the role of estrogen signaling in the regulation of metabolic-driven inflammatory process at the basis of NAFLD development and progression. The gene discussed is GH1; the disease is metabolic dysfunction-associated steatotic liver disease.