This report highlights the distinct phenotypes of two mouse myogenic tumor models – those initiated by combined Cdkn2a (p16p19) disruption and Kras expression in transplanted mouse muscle satellite cells (10) and those arising in the skeletal muscle of mice with activated Hh signaling due to expression of a mutant, constitutively active smoothened (SmoM2) allele (11, 12). Here, KRAS is linked to neoplasm.