Gentamicin significantly induces apoptosis in NRK-52E cells in a dose-dependent manner, whereas pretreatment with TMP inhibits the release of cytochrome c, inhibits the activation of caspase-3/8/9, increases the expression of Bcl-XL, inhibits the activation of NF-κB, and reduces ROS production, suggesting that TMP may be able to inhibit apoptosis and inflammatory and oxidative stress processes to relieve tubular injury in GM-AKI (Juan et al., 2007). The gene discussed is NFKB1; the disease is acute kidney injury.