The etiology of BCC is based on the persistent ligand‐independent activation of hedgehog/glioma‐associated oncogene homolog (HH/GLI) signaling, caused in the vast majority of cases by inactivating mutations in the HH receptor and pathway repressor Patched‐1 (PTCH1) or in fewer cases by activating mutations in the essential HH effector Smoothened (SMO). This evidence concerns the gene GLI1 and skin basal cell carcinoma.