Increased expression of PRSS23, CDH6, and LYPD1 with IFN-γ treatment, which also robustly induced the IFN-induced transmembrane protein 1, suggested a shift in the total podocyte population toward EGE gene expression and possible dedifferentiation relevant to glomerular disease (Figure 4A).50,51. The gene discussed is PRSS23; the disease is glomerular disorder.