Given that CaMKII is indicated as an upstream kinase that directly phosphorylates and activates TAK133,34, and considering our observation that obesity-induced CaMKII activation in adipocytes can be nullified by TRPM7 knockdown or channel activity inhibition, we propose that the activation of CaMKII under a TRPM7-mediated event is the essential Ca2+-signaling component of this pathway. This evidence concerns the gene CAMK2G and obesity due to melanocortin 4 receptor deficiency.