Critically, aberrantly glycosylated IgA1 isolated from the serum of IgA nephropathy patients induces NLRP3 expression in cultured podocytes and upregulates F4/80—a macrophage lineage marker—concomitant with increased expression of the adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) and the fibrotic marker α-smooth muscle actin (α-SMA). The gene discussed is NLRP3; the disease is IgA glomerulonephritis.