CDKN2A and neoplasm: According to a finding by Peyre et al., homozygous and heterozygous Cdkn2a/b deletions together with biallelic Nf2 inactivation contribute to increased meningioma frequency with a shorter latency in mice, while single Cdkn2a/b inactivation hardly leads to tumor development, indicating that Nf2 and Cdkn2a/b cooperate to promote meningioma progression96.