It has been demonstrated that ischemia markedly increased the Bax/Bcl-2 ratio in a proapoptotic direction and caspase-3 activation was the predominant mechanism underlying the pathogenesis of I/R-induced tubular cells apoptosis.9,26 These data further confirmed that renal tubular epithelial cell apoptosis induced by I/R injury played a key role in the development and progression of AKI. The gene discussed is BCL2; the disease is acute kidney injury.