Abnormal stimulation of the PI3K/Akt pathway is related to tumor growth, angiogenesis, and survival [11], in which the loss of function of tumor suppressor gene phosphatase and tensin homolog deleted on chromosome ten (PTEN) is commonly seen in human tumors and leads to the stimulation of the PI3K/Akt pathway [12]. Here, AKT1 is linked to neoplasm.