However, as TGFβ has been shown to drive the progression of colon cancer via its effects in the tumor microenvironment, we bred APC to those with global TGFβ signaling deficiency (Tgfbr1+/− or TG) to form ATG, which more closely mimics the effects of systemic administration of a TGFβ inhibitor, the majority of which target TGFBR1 (Figure 2c). Here, APC is linked to neoplasm.