These results indicated that the balance between survival and death signals in lung cancer cells was disrupted by the decrease in p-PI3K, p-AKT, and p-ERK levels and the increase in p-JNK levels caused by β-lapachone treatment, and that NQO1 expression and activity were involved in the activation of all these apoptotic signals. The gene discussed is AKT1; the disease is lung carcinoma.