To check whether the downstream p21 suppression in this potential ER stress/JNK/caspase-3 axis (due to 3-AWA treatment) is independent of the cellular status of p53, we used isogenic HCT-116 p53+/+ and HCT-116 p53−/− colon cancer cells. The gene discussed is TP53; the disease is malignant colon neoplasm.