Cancer can result from any number of abnormalities in the control of cell-cycle progression, intracellular signaling and transduction of extracellular cues. Many insights into the crucial events that govern the regulation of cell growth have derived from studies of the gene products mutated in inherited cancer syndromes. Recent work on the neurofibromatosis 2 (NF2) tumor suppressor gene suggests that this negative growth regulator might function by modulating growth factor and extracellular matrix (ECM) signals that trigger Rac1-dependent cytoskeleton-associated processes. In this article, we propose a molecular model for NF2 protein (merlin) function in the light of these and related new findings.