Misra et al. (321) showed that both constitutive activation of ErbB2 and ligand-mediated activation of IGF1R-β and PDGFR-β are reversed by co-treatment of the cancer (colon, prostate, and breast) cells with a HA antagonist, and concluded that HA serves a general function in receptor tyrosine kinase (RTK) activation. The gene discussed is NTRK1; the disease is cancer.