Therefore, in addition to Igf1r, we observed alterations in levels of Grb10 and Inpp4a, two checkpoint molecules critical for keeping AKT activity balanced; we hypothesized that diabetes and MAO inhibition could impact the IGF1R/PI3K/AKT signaling axis downstream of the IGF1R to affect the activation of pro-survival signaling pathways. The gene discussed is IGF1R; the disease is diabetes mellitus.