Of the 12 tumors analyzed, we identified 6 embryonal rhabdomyosarcomas (ERMSs) harboring mutations in key signaling molecules (KRAS, HRAS, NRAS, and FGFR4), oncogenic DICER1 mutations in 2 ERMS, pathogenic TP53 and NF1 mutations in an ERMS with features of anaplasia, a TEAD1::NCOA2 gene fusion in a congenital spindle cell and sclerosing rhabdomyosarcoma (SSRMS), and a FUS::TFCP2 gene fusion in a skull base SSRMS. This evidence concerns the gene TEAD1 and embryonal rhabdomyosarcoma.