Although activation of the Hh pathway by somatic mutations is rare in breast cancer [55,56], non-canonical Hh activation through transcriptional upregulation of GLI1 is seen downstream of multiple oncogenic pathways, including the PI3K-Akt-mTOR pathway [40], K-Ras, c-Myc, Wnt-beta catenin and TGFβ [57]. This evidence concerns the gene GLI1 and breast cancer.