Repression of SMO is lessened by allowing dissociation from SUFU, which leads to the translocation of full-length GLI2 into the nucleus and activates transcription of HH target genes, promoting ovarian cancer cell proliferation, survival, and invasiveness (starting with the activation of PTCH1 receptor onto HH ligand binding) [60] (Fig. 3). This evidence concerns the gene SMO and ovarian carcinoma.