RB1 and neoplasm: While biallelic inactivation of NF1 in CN is traditionally felt to be necessary for tumor development, somatic mutations affecting other tumor suppressor genes, (TP53, CDKN2A and RB1) have been identified in NF1 associated tumors including CN, suggesting that modifying loci may be sufficient for tumor growth in the absence of a second NF1 mutation, or that the acquisition of a mutation at a modifying loci, in addition to a second NF1 hit, may be a one of the factors affecting tumor growth behaviors[7].