The tumor latency in these rats is substantially faster than tumor latency in rats with a germline deletion of one copy of Nf1 (18 days vs. 70–90 days depending on the line)15, suggesting that somatic mutations of Nf1 are potent in initiating cancer and that homozygous mutations are likely more transforming than heterozygous mutations which may require loss of heterozygosity to complete tumorigenesis. This evidence concerns the gene NF1 and neoplasm.