In order to better understand the metabolic adaptations that enable the outgrowth of soft-tissue sarcomas (STS), we utilized a genetically engineered mouse model that mimics rhabdomyosarcoma (RMS) that we previously characterized whereby intramuscular injection of 4-hydroxytamoxifen activated a muscle satellite cell-specific CreERT2 to turn on expression of an oncogenic NrasG12D allele and delete both p53 alleles24, resulting in local tumor formation (P7NP sarcoma) within 4–6 weeks (Fig. 1a). The gene discussed is TP53; the disease is neoplasm.