SMAD3 and neoplasm: The transforming growth factor β (TGFβ) pathway has recently been shown to exhibit aberrant activation in human NSCLC patient tissues, mediated by epigenetic silencing of the pseudo-receptor BMP and activin membrane-bound inhibitor (BAMBI) that resulted in increased Mothers against decapentaplegic homolog 3 (SMAD3) phosphorylation, tumor growth, and Epithelial-Mesenchymal-Transition (EMT) signatures (5).