Moreover, the inactivation of ILK downstream target GSK3β, either via transgenic depletion or by Serine 9 phosphorylation, correlates with exacerbated kidney damage in multiple AKI and CKD models, both in vitro and in vivo, by mechanisms related to mitochondrial metabolism and permeability, transcriptional regulation, oxidative stress and tubular epithelial cells survival [15,16]. The gene discussed is ILK; the disease is Nephropathy.