Given the role for the cell cycle inhibitor and putative tumor suppressor CDKN1C in controlling the switch between myogenic proliferation and differentiation [38], and the mutation of CDKN1C in the childhood imprinted disorders Costello syndrome and Beckwith‐Wiedemann syndrome (at risk of developing FN‐RMS [26, 39, 40]), we focused on CDKN1C and assessed whether it might be downstream of YAP1 in our system. The gene discussed is CDKN1C; the disease is Costello syndrome.