NAM is also a feedback inhibitor of NAD+-dependent enzymes, and high concentrations of NAM inhibit the activity of poly (ADP-ribose) polymerase (PARP), sirtuins, and CD38 [46], resulting in an increase in accumulation of hepatic fat [47,48], insulin resistance [49], and spatial-learning deficits [50]. The gene discussed is CD38; the disease is Insulin resistance.