LLGL2 and colorectal cancer: We engineered human DLD1 epithelial colorectal cancer cells to overexpress either WT GFP–Llgl2 or variants harboring interface substitutions that we characterized in the kinase-docking DPYSD motif (Llgl2DPYSD>RPYSR), the PBM motif (Llgl2IE>NE) and the substrate-docking LSR motif (Llgl2LSR>ASA).