TGFβ and BMP interplay in tumor dormancy, growth and invasion. (a) TGFβ and BMPs pathways can cooperate to induce tumor dormancy. However, non-canonical TGFβ-activated PI3K/AKT signaling can promote the exit from dormancy and re-enable tumor cell proliferation. (b) TGFβ and BMPs play prevalently counteractive roles in tumor cell growth and invasion. The TGFβ/SMAD2 axis may induce cell cycle arrest in early phases of tumorigeneses (such as in HCC). However, at later tumor stages SMAD-independent TGFβ signaling is suggested to promote events that result in cell growth enhancement, the EMT, and invasiveness. Overall BMPs act to limit tumor cell proliferation and invasion, and TGFβ tumor-promoting actions may rely on the offsetting of BMPs dependent signals. Tumor limiting/promoting ligands are enclosed in green/orange boxes, respectively.