,8 The etiology of complement dysregulation in C3G may be genetic susceptibility (e.g., susceptible haplotypes or pathogenic mutations), autoimmunity such as autoantibodies against complement regulatory factors, or other environmental factors.1, 2, 3, 4, 5, 6, 7,9, 10, 11 Dysregulation of the complement system in these glomerular diseases, especially in C3G, results in amplification and propagation of the complement cascade, including downstream membrane attack complex (C5b-9) assembly (Figure 1), culminating in glomerular deposition of C3 and C5 breakdown products and kidney injury.4 This evidence concerns the gene RAPGEF1 and glomerular disorder.