In this context it is noteworthy that the immune-modulatory drug imiquimod is already successfully used for the treatment of superficial BCC [58, 93] by boosting T-cell effector function, although there are other reports suggesting an additional therapeutic role of imiquimod such as by directly blunting oncogenic HH/GLI via activation of adenosine receptor/protein kinase A (PKA) signaling and by activating tumor-killing plasmacytoid dendritic cells [94–97]. Here, GLI1 is linked to neoplasm.