Previous evidence has demonstrated the binding of calmodulin (CaM) to NMDARs is required for CaM-dependent inactivation of NMDAR, and NMDARs-mediated CaMKII/ERK activation contributes to renal fibrosis [17, 18], indicated CAM, CAMKII, and ERK pathways are essential for NMDARs regulated cell function. This evidence concerns the gene CAMK2G and renal fibrosis.