In addition, (S)-crizotinib inhibits gastric cancer cell growth through oxidative DNA damage mechanism and can trigger survival promoting AKT signal at the same time, which increase the growth rate γ-H2AX and Ser1981 phosphorylated ataxia telangiectasia-mutated gene, while N-acetyl-l-cysteine could inhibit this effect of (S)-crizotinib. The gene discussed is AKT1; the disease is gastric cancer.