While greater than 90% of the incidence of small cell lung cancer is the result of unchecked proliferation due to acquired mutations in RB1, development of NSCLC is attributed to the accumulation of mutations in genes involved in the upstream regulation of the retinoblastoma protein (RB), such as TP53 (encoding the tumor protein p53), CCND1 (encoding the G1/S-specific cyclin D1), and CDKN2A (encoding the cyclin-dependent kinase inhibitor (CDKI) p16INK4a) [2]. Here, CDKN2A is linked to non-small cell lung carcinoma.