In early work elucidating the role of microenvironment on tumor dormancy, Aguirre-Ghiso and colleagues showed that growth signals from fibronectin (an extracellular matrix (ECM) protein) via the urokinase plasminogen activator receptor (uPAR)-α5β1-integrin complex was critical, and thus reduction in the level of uPAR in human epidermoid cancer cells induced tumor dormancy when tested using standard tissue culture polystyrene (TCPS) substrates (routinely employed two dimensional (2D) culture models) in vitro as well as using mouse models in vivo [15]. This evidence concerns the gene FN1 and neoplasm.