Mechanisms in tumors involves HH pathway can be described as 3 aspects [5]: (1) This pathway is activated by either functionally deficient mutations in inhibitory proteins (such as PTC1, SUFU) or functionally acquired mutations in positive regulators (such as SMO); (2) Overexpression of HH ligands acting in an autocrine/paracrine function to activate the HH pathway, and result in a feedback mitogen that induces tumor growth; (3) Overexpression of HH ligands leads to the regeneration of tumor stem cells. This evidence concerns the gene SMO and neoplasm.