In autochthonous mouse models of small cell lung cancer (SCLC), overexpression of SHH or SMOM2, a constitutively active mutant, in Rb−/−;Trp53−/− cancer cells promoted tumor proliferation [26, 27], loss of SMO led to significantly decreased tumor formation, and treatment with sonidegib inhibited tumor growth of chemotherapy-resistant SCLC in vivo [26]. Here, SMO is linked to neoplasm.