In view of reports that human NF1 tumor cells exhibit constitutive activation of N- and K-Ras, but little or no H-Ras [146], and that the N-Ras activation in NF1 tumor cells drives ERK MAP kinase activation and transcriptional reprogramming [147, 148], it may not be surprising that tipifarnib did not produce significant benefit. This evidence concerns the gene NRAS and neoplasm.