The “GLI1” level hypothesis in cSCC and BCC development together with our observation that low levels of GLI1 expression seem to be associated with cSCC initiation could also explain the observation that treatment of BCC with vismodegib, which usually inhibits canonical HH signaling pathway by binding to SMO, can result in cSCC development (see e.g. Ransohoff et al., 2015; Mohan et al., 2016). The gene discussed is GLI1; the disease is skin squamous cell carcinoma.