In further support of this hypothesis, mice with a combined deficiency of inhibitor of differentiation 3 (Id3) and ApoE−/− spontaneously develop glomerulonephritis characterized by lipid deposition specifically in glomeruli, the presence of enlarged hypercellular glomeruli, mesangial expansion, and increased extracellular matrix deposition (71). This evidence concerns the gene ID3 and glomerulonephritis.