Thus, modulation of PKA activity by the mtCB1 receptor might not only underlie impairment in mitochondrial respiration but also result in perturbed AKAP-PKA trafficking, which might finally lead to altered substrate utilization in adipocytes, a phenomenon consistently observed in pathological conditions such as obesity and metabolic diseases [67]. The gene discussed is AKAP1; the disease is obesity due to melanocortin 4 receptor deficiency.