Given that NAFLD and T2D are concurrent comorbidities characterized by hepatic steatosis, glucose intolerance, and insulin resistance (Tilg et al., 2017), we explored whether loss of Slc39a5 and consequent hepatic zinc accumulation (Figure 2B) influenced liver function in models of congenital obesity and diet-induced obesity. The gene discussed is SLC39A5; the disease is metabolic dysfunction-associated steatotic liver disease.