While several signaling pathways, including those driven by STAT3, Hedgehog/Gli1, and Wnt/β-catenin, are known to be active in bladder CSCs, the sustenance of their stem-like properties is intricately regulated by a combination of intrinsic signaling cascades and extrinsic cues from tumor microenvironment (TME) and the broader tumor macroenvironment (TMaE) 8-12. Here, GLI1 is linked to neoplasm.