It is now known that in the pathophysiology of IgA nephropathy (IgAN), the cytokines BAFF and APRIL play a key role in supporting B cell survival, increasing Gd-IgA1 synthesis, and promoting immune complex deposition in the mesangia, thereby accelerating damage to the glomerular [26] similar to obesity [27,28,29]. The gene discussed is IGHA1; the disease is obesity due to melanocortin 4 receptor deficiency.