In lung cancer cells, SHH is overexpressed and competitively binds PTCH leading to its dysfunctions in arresting SMO activation followed by upregulation of GLI1 which consequently induces the transcription activities of GLI1 target genes including Hedgehog cascade members (SHH, PTCH, and GLI1) and cell cycle components (Cyclins and CDKs). This evidence concerns the gene SHH and lung carcinoma.