Small‐molecule SMO inhibitors (SMOi) show striking therapeutic efficacy in patients with advanced and metastatic BCC,7, 8 though development of drug resistance and severe adverse effects leave many patients without proper treatment options.9, 10, 11 Furthermore, noncanonical, SMO‐independent GLI activation has been identified as critical factor contributing to the growth of malignant cells refractory to SMOi treatment (reviewed in Refs. This evidence concerns the gene GLI1 and skin basal cell carcinoma.