Notably, targeted pathway inhibition has shown clinical success particularly in HH‐driven basal cell carcinoma (BCC) and medulloblastoma.1, 2 However, rapid and frequent development of resistance to HH inhibitors urgently calls for additional treatment options.3 Canonical HH/GLI signaling is initiated by the binding of secreted HH protein to Patched (PTCH), a transmembrane domain protein that represses HH signaling in its unliganded state by inhibiting the ciliary localization and activation of the essential HH effector Smoothened (SMO). Here, GLI1 is linked to basal cell carcinoma.