Sarcomas are clinically, histologically, and molecularly heterogeneous, with at least 70 distinct subtypes occurring in bone and soft tissues.1 Molecular alterations most commonly involve tumor suppressors (eg, cell cycle control genes, TP53), DNA damage response genes, epigenetic regulators, and, rarely, receptor tyrosine kinases (RTK).2,3 The prevalence of a given class of alterations varies widely among histologic types. This evidence concerns the gene TP53 and sarcoma.