CCL2 and IgA glomerulonephritis: demonstrated that both Tnfrsf11 and Tnfrsf11a are overexpressed in glomeruli and tubulointerstitium, concomitant with NF‐κB activation and elevated CCL2.[78] In human glomerular diseases such as focal segmental glomerulosclerosis, IgA nephropathy, and membranous nephropathy, podocyte and mesangial cells upregulate Tnfrsf11a.[79] Our findings establish Tnfrsf11a+ Mφ as key regulators of kidney inflammation via Zc3h12c‐dependent RNA splicing.