Here, the DEP domain of Dvl binds to the C-terminus of Vangl1, creating a functional Vangl1-Dvl-PKCδ tertiary complex that mediates downstream signaling events through Erk/AP-1 and drives actin cytoskeletal rearrangements to promote CRC invasiveness (Kho et al., 2009). This evidence concerns the gene JUN and colorectal carcinoma.