Several factors could contribute to the different effects of constitutive vs. pharmacological Nrf2 activation on cancer cell growth, including the magnitude and duration of Nrf2 target gene expression [52]; the levels of other Keap1-interacting proteins, such as IKKβ and BCL2 [53–55]; and AIM-mediated activation or inhibition of other pathways that affect cancer cell survival, such as IKKβ (NF-κB), STAT3, JNK, Cyclin D1, CDKN1A (p21) [9,10]. The gene discussed is STAT3; the disease is cancer.