Advanced cancers such as gliomas, breast and prostate cancers usually do not acquire mutations in the core components of TGF-β/SMAD signaling, but can bypass the TGF-β/SMAD tumor-suppressive arms through other, more downstream (epi)genetic changes, allowing the tumor promoting arm of TGF-β/SMAD signaling to actively drive tumor cell progression (Jennings and Pietenpol, 1998; Jones et al., 2009; Takenoshita et al., 1998; Vincent et al., 1996; Xu et al., 2009). This evidence concerns the gene TGFB1 and neoplasm.