The exact mechanism behind Shh maintaining the CSC self-renewal capabilities is unknown; however, studies performed on thyroid cancer [76,77,78,79], embryonal RMS [80], and breast cancer [81] revealed that increased Shh and SMO signalling lead to increased expression of SOX2, NANOG, OCT3/4, and KLF4 transcription factors. This evidence concerns the gene SOX2 and breast cancer.