Although the t(9;12)(p22;q14 ~ 15) thus appears to be heterogeneous at the molecular level, generating HMGA2-NFIB in pleomorphic adenoma and lipomas but HMGA2-C9orf92 in the only myolipoma examined, the pathogenetic pattern behind these changes is similar to that of HMGA2 rearrangements found generally in benign connective tissue tumors, i.e., disruption of the HMGA2 locus leaving intact exons 1–3 which encode the AT-hook domains and separates them from the 3 ́-untranslated region of the gene (3 ́-UTR) [20]. This evidence concerns the gene NFIB and connective tissue neoplasm.