MET and colon adenocarcinoma: As c-Met is a known intrinsic modulator of CSC self-renewal, eliciting a genetic program known as invasive growth6–11, and the c-Met ligand HGF is secreted by stromal myofibroblasts in colon adenocarcinoma to activate the self-renewal pathway to sustain long-term CSC propagation23, we chose to focus on the c-Met inhibitors identified in our compound screen.