Given our previously published findings that constitutive deletion of KIBRA in mice was protective against acute podocyte injury (20) and our in vitro demonstrations of KIBRA-induced structural derangements, we next hypothesized that KIBRA overexpression in vivo would either directly lead to a glomerular disease phenotype or would enhance susceptibility to acute and chronic glomerular injury. This evidence concerns the gene WWC1 and glomerular disorder.