In human renal cell carcinoma lines, sonidegib inhibited GLI1 and GLI2 and reduced cell proliferation in combination with everolimus or sunitinib, whereas direct inhibition of GLI1 and GLI2 in combination with everolimus or sunitinib had no impact on proliferation, suggesting that other targets downstream of SMO may play a role in tumor response [24]. The gene discussed is SMO; the disease is renal cell carcinoma.