JNK exhibits pro-survival function in cancer cells due to its ability to enhance the processes of proliferation, migration, and invasion through a plethora of mechanisms, including synergistic action with p38 MAPKs and nuclear factor kappa B (NF-κB), the upregulation of antiapoptotic gene expression such as BCL2, and the blockade of caspase activation [23,47,48,49]. The gene discussed is BCL2; the disease is cancer.