This is in line with an earlier study ruling out SHH autocrine signaling in ERMS patients.6 Pathway inhibition was effective at the level of SMO as well as of GLI, which could avoid emergence of cross talks converging on the GLI-code and resistance mechanisms in the clinics.9 Furthermore, we found that modulating the pathway can alter sensitivity to generic drugs. This evidence concerns the gene GLI1 and embryonal rhabdomyosarcoma.