Notably, silencing of the c-MET receptor inhibited cell proliferation, and increased apoptosis in both ARMS- and the fusion-negative ERMS-derived cell lines, which underscores a role for the HGF/c-MET pathway in RMS beyond the effects of the PAX3-FOXO1 transcription activator found largely in ARMS. The gene discussed is MET; the disease is alveolar rhabdomyosarcoma.