We compared this new model to a well-established ERMS GEMM that relies on satellite cell-specific activation of oncogenic KrasG12D and loss of the tumor suppressor Trp53 to drive tumor formation (Pax7CreER/+; KrasLSL-G12D/+; Trp53fl/fl) [13,14,15,16,17]. This evidence concerns the gene TP53 and neoplasm.