However, as determined in SMO inhibition assays, these axes promote the down-regulation of GLI-1 gene expression and facilitate significant EGFR-TKI-based treatment susceptibility, thereby reducing tumor cell proliferation in both EGFR-wild type as well as EGFR-mutated NSCLC cell lines [51], suggesting an interdependent oncogenic addiction between the EGFR and SHH-GLI1 axis pathways that is involved in lung cancer cell survival and cancer drug resistance [52]. This evidence concerns the gene SMO and neoplasm.