We first assessed whether the DNA damage response is the basis for growth arrest in response to low-dose Aza treatment in our panel of melanoma cell strains, because Aza at even 0.1 μM can induce DNA damage in human lung cancer cell lines [20]–[23], and concentrations of ∼1 μM and above also activate p53, resulting in p21Cip1 induction and cell cycle arrest [20]–[22]. The gene discussed is CDKN1A; the disease is lung cancer.