Looking at the several important roles of the Nrf2/HO-1 pathway, such as suppression of oxidative stress and inflammation, improvement of insulin resistance [166], inhibition of phosphorylation of PI3K/Akt [165, 167], inhibition of NF-κB [165], as well as their individual suppressive role (independent of each other) on FFA-induced ED [132, 178], it could be endorsed that the pathway could be an avenue for future therapy for FFA-related ED (Fig. 2). The gene discussed is AKT1; the disease is Insulin resistance.