Consistently, previous studies have also reported that AKAP1 deficiency did not affect cardiovascular and renal functions under basal conditions.[30, 31, 32] In comparison, in mice subjected to different disease models, AKAP1 deficiency exacerbates cardiovascular, lung, and cerebral vulnerability.[30, 31, 32, 33, 34, 35] These findings suggest that AKAP1 could be a safe therapeutic target for the treatment of obesity under specific physiological conditions. The gene discussed is AKAP1; the disease is obesity due to melanocortin 4 receptor deficiency.