The use of a stabilized form of BCL9 α-helix (SAH-BCL9) is also suggested in potential therapy, as its administration caused dissociation of the native β-catenin/BCL9 complex as well as suppressed tumor growth and angiogenesis in the mouse xenograft model of the Colo320 CRC cell [83]. The gene discussed is BCL9; the disease is colorectal carcinoma.