In a clinical trial on patients with IgA nephropathy, the investigators found that toll-like receptor 7 (TLR7) can activate B cells through the TLR7- GALNT2 axis, which produces high levels of galactose-deficient IgA1 (Gd-IgA1) (53). This evidence concerns the gene IGHA1 and IgA glomerulonephritis.