Numerous preclinical studies have suggested that genistein increases SOD protein expression by upregulating the Nrf2 pathway and the PI3K/Akt pathway as well as downregulating the mitogen-activated protein kinase (MAPK) pathway, especially jun N-terminal kinase (JNK) and p38 MAPK, which decreases the prevalence of aging, AD, PD, CVD, and cancer (e.g., bladder cancer, liver cancer, and breast cancer) induced by ROS [7]. The gene discussed is AKT1; the disease is cancer.