TGFB1 and neoplasm: Similarly, we found significantly more functional interactions among the kinases identified as dependencies associated with mutation of the tumor suppressor SMAD4, a member of the TGF-β pathway that is frequently mutated or homozygously deleted in colorectal (Thiagalingam et al., 1996), pancreatic (Hahn et al., 1996), and esophageal (Dulak et al., 2013) cancers (Figure 4B).