These include attenuation of cytokine- and growth factor- induced oncogenic signaling via JAK and receptor tyrosine kinases (RTK) (55–58), potentiation of p53-mediated tumor suppressor functions (59, 60), inhibition of the paradoxical oncogenic functions of tumor suppressors such as cyclin-dependent kinase inhibitor 1A (CDKN1A; commonly known as p21Cip1/WAF1) and NFE2 Like BZIP Transcription Factor 2 (NEF2L2; commonly known as Nuclear factor erythroid 2-related factor 2 or NRF2) (52, 53, 61, 62). The gene discussed is CDKN1A; the disease is neoplasm.