For instance, upregulation of p22phox was reported to activate both PI3K/Akt and ERK1/2 pathways and induce HIF-1α via ROS signaling in prostate cancer [16]; overexpression of p22phox was also reported to cause diminishing the entry of CDDP into the nuclei followed by an inhibition of apoptosis and drug resistance in oral squamous cell carcinoma [20]; EMT was also reported to be induced when p22phox expression was increased by exposure to tobacco smoke extract in NSCLC [17]. Here, AKT1 is linked to oral cavity squamous cell carcinoma.