In order to investigate the impact of oncRAS mutations on non-canoncial HH/GLI signaling activity in established human sporadic ERMS, the RAS wildtype ERMS cell lines RUCH-2 and TE617.T were stably transduced with pMSCVpuro-HRASG12V, pMSCVpuro-KRASG12V, pMSCVpuro-NRASG12V, or the pMSCVpuro empty vector (HRAS, KRAS, NRAS, or pMSCV, respectively). This evidence concerns the gene NRAS and embryonal rhabdomyosarcoma.