TGF-β signaling leads to opposing effects depending on activin receptor-like kinase-1 (ALK-1) and activin receptor-like kinase-5 (ALK-5) activity, which may lead to either inhibition or stimulation of proliferation, migration, and angiogenesis [22,23] in the same ambiguous way that TGF-β mediates most, if not all, tumor processes. The gene discussed is ACVRL1; the disease is neoplasm.