Likewise, Mathew et al. [47] generated a “super Ink4a/Arf” mouse strain carrying a transgenic copy of the entire Ink4a/Arf locus and demonstrated that modest increase in the activity of the Ink4a/Arf tumor suppressors also resulted in a beneficial cancer-resistant phenotype without affecting normal viability or aging. The gene discussed is CDKN2A; the disease is neoplasm.