Early research links the HGF/c-MET pathway to development of RMS; c-MET was identified as a target of the PAX3-FOXO1 fusion protein (55), and a murine model of RMS showed that dysregulation of HGF/c-MET signaling on the background of suppression of INK4a/ARF (locus that encodes two tumor suppressors) was sufficient to lead to the development of RMS tumors with a similar molecular signature to human RMS tumors (56). The gene discussed is HGF; the disease is neoplasm.