They demonstrated that GLI1, that is upregulated at the tumor-stroma intersection in HNSCC, is increased by RT, where it contributes to stroma-mediated resistance, and that HH inhibition offers a rational strategy to reverse this process and to sensitize HNSCC to irradiation (Gan et al., 2014). The gene discussed is GLI1; the disease is head and neck squamous cell carcinoma.