To date, inhibition of HMGCR by statins has been shown to promote cell apoptosis in RMS [[27], [28], [29], [30], [31]], as well as inhibition of RAS farnesylation by tipifarnib, a potent and selective farnesyltransferase (FTase) inhibitor, was sufficient to produce tumor growth inhibition exclusively in HRAS-mutant RMS xenografts [32]. This evidence concerns the gene HMGCR and neoplasm.