Recently, Tanaka et al. [16] have proposed a central role of hypoxia in the AKI to CKD transition, and have hypothesized that after functional recovery from the early phase of AKI, the expression of vascular factors, such as vascular endothelial growth factor (VEGF) in tubular cells, is not yet restored, which results in capillary rarefaction leading to renal hypoxia, and consequently activation of inflammatory reactions, induces myofibroblast migration and/or differentiation and damages the regenerated tubules. The gene discussed is VEGFA; the disease is acute kidney injury.