Collectively, all the data above suggest that SBE-mediated selective targeting inhibition of SHH-cell cycle signal axis in lung cancer therapy is achieved via its direct and selective inhibition of SMO at both transcriptional and translational levels which consequently leads to significant inhibition of GLI1 and its downstream targets including SHH signaling components and cell cycle regulators (Fig. 6D). Here, SMO is linked to lung carcinoma.