In line, an ADAM10‐dependent increase in Wnt‐responsive genes following antibody‐mediated podocyte injury are described in vitro and in vivo together with enhanced beta‐catenin levels and beta‐catenin translocation to podocyte nuclei, supporting a role of the Wnt‐signaling pathway in mediating podocyte cell adhesion during glomerulonephritis [528], downstream of ADAM10‐mediated N‐cadherin shedding [529]. This evidence concerns the gene CTNNB1 and glomerulonephritis.