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). Here, SMAD4 is linked to cancer.