Additionally, given published data showing that YAP can inactivate glycogen synthase kinase 3β (GSK3β) (38) and that loss of GSK3β ameliorates ADR-induced nephropathy with preservation of actin integrity and reduced activation of paxillin (39), it is possible that increased activity of GSK3β in the setting of KIBRA-induced YAP inhibition may also contribute to the significant injury susceptibility observed with KIBRA overexpression. Here, PXN is linked to kidney disorder.