CD155, expressed on the surface of cancer cells, was shown to promote tumor invasiveness.42 Its upregulation in tumor environment–infiltrating myeloid cells restrained anti-tumor immunity by impairing anti-tumor T lymphocyte and NK cell function.43 hsBCL9CT-24 treatment increased mRNA expression of CD155/Pvr in CT26 cells (Fig. 6j), while Bcl9 depletion in CT26 similarly increased expression of CD155/Pvr (Fig. 6k). Here, BCL9 is linked to neoplasm.