Prior studies have shown that XLID-linked MED12 mutations lead to inactivation of MED12 protein function which subsequently promotes dysregulation of GLI3 signaling [26] Since the mutations found in XLID syndromes closely cluster to the prostate cancer associated MED12 mutations we presume that these mutations similarly lead to inactive MED12 protein function. This evidence concerns the gene GLI3 and prostate carcinoma.