In our previous studies, we have demonstrated that activation of PI3K/Akt can reduce the expression of the phosphoric acid lipases, PP1, PP2A, and SSH, then activate the de-phosphorylation of p-cofilin-1 and mitochondrial translocation of cofilin-1 and finally activate mitochondrial damage and induce the mitochondrial apoptosis of cisplatin-resistant gastric cancer cells (Tang et al., 2016). The gene discussed is AKT1; the disease is gastric cancer.