Furthermore, detailed phenotypic analysis of mammaryfibroblasts derived from Cav-1 (-/-) null mice revealed that they sharenumerous properties with cancer-associated fibroblasts, such as constitutivelyactive TGFbeta signaling, and that they have the ability to promote normalmammary epithelial cells to undergo an EMT (epithelial-mesenchymal transition)[2]. The gene discussed is CAV1; the disease is cancer.