Our observations that Bcl3 knockdown inhibits Shh signaling and blocking Shh signaling with multiple agents diminishes Bcl3-dependent signaling point toward meaningful crosstalk between the Shh and Bcl3-dependent signaling pathways in the pathogenesis of BCCs in this murine model and potentially in NBCCS patients. The gene discussed is BCL3; the disease is nevoid basal cell carcinoma syndrome.