A number of additional, recurrent genetic abnormalities are found, including the loss of major tumor suppressive pathways (e.g., inactivating mutations of PTEN and of the CDKN2A tumor suppressor locus) and activation of oncogenic pathways (e.g., activating mutations in NOTCH1/FBXW7, IL7R/JAK pathway, epigenetic regulators, cell cycle, PI3K, and RAS signaling) [9–12]. This evidence concerns the gene CDKN2A and neoplasm.