Established evidence from lipodystrophy syndromes, “lipodystrophy-like” phenotypes and genome-wide association studies consistently demonstrates that true leptin deficiency states are associated with increased metabolic dysfunction and hepatic steatosis because in this context leptin represents a biomarker for reduced functional adipose tissue mass causing excess calories to be stored in ectopic sites which drives lipotoxicity and insulin resistance [16, 17]. This evidence concerns the gene LEP and steatosis.