An intriguing hypothesis emerging from the data reviewed so far is that Ad-36 could be involved in the genesis of hepatic steatosis/NAFLD by reducing leptin gene expression—as feedback mechanism—and insulin sensitivity, by increasing glucose uptake, by activating the lipogenic and pro-inflammatory pathways in adipose tissue, and by increasing the level of macrophage chemo attractant protein-1, ultimately leading to chronic inflammation and altered lipid metabolism [66]. The gene discussed is LEP; the disease is metabolic dysfunction-associated steatotic liver disease.