Cytokines, such as tumor necrosis factor (TNF), mediate decisive interactions between the cancer and stroma, with characteristic experiments performed at the lab of Ben-Baruch demonstrating that TNF-induced NFκB p65 RelA and TGFβ1-induced SMAD3 acted in parallel in mesenchymal cells to activate the expression and release of factors that affect other cells in their microenvironment and induce breast tumor cell elongation, migration, and scattering out of spheroid tumor masses [159,160]. The gene discussed is SMAD3; the disease is cancer.