Our data suggest that these KIBRA-promoted effects are mediated to a large extent via YAP inhibition, given the findings of cytoplasmic YAP localization in KIBRA-OE human podocytes with a very apparent injury phenotype at baseline and of both increased phosphorylated YAP and reduced nuclear/increased cytoplasmic YAP in KIBRA-OE mice with heightened susceptibility to acute PS-induced FP effacement and ADR-induced FSGS. This evidence concerns the gene WWC1 and focal segmental glomerulosclerosis.