Considering that: (1) MO results in distorted angiogenesis; (2) obesity has been associated with ER stress and IR; and (3) IR-related proteins also play a role in cell migration (RhoA, Akt), we hypothesize the possible contribution of different IR-related and others proteins to the modulation of EC migration capacity in the context of MO-dependent ER stress (Table 1). The gene discussed is AKT1; the disease is obesity due to melanocortin 4 receptor deficiency.