Furthermore, SHH-GLI1 signaling inhibition is involved in sensitization to EGFR-TKI (gefitinib/erlotinib)-based therapy, thereby reducing cellular viability, as well as the self-renewal function of cancer stem-like cells derived from the EGFR-mutated lung cancer cell lines H1650 and H1975 [31]. This evidence concerns the gene SHH and lung cancer.