In this context, SGLT2i alleviated DN in experimental and clinical studies by diminishing the expression of SREBP-1 lipogenic molecule with the levels of pathogenic adipokines, leptin and resistin, whilst increasing adiponectin levels and promoting the expression of PPARα and PPARγ lipolytic molecules, thus inhibiting renal lipotoxicity, oxidative stress, and inflammation [15,20,43,44]. The gene discussed is LEP; the disease is liver dysplastic nodule.