Proposed role of Vav3 in formation of the macrophage phagocytic synapse and its implications in wound regeneration. Based on the study by Sindrilaru et al, Vav3 stimulates a bidirectional signal to control (1) the avidity of CD18/β2 integrin toward ICAM on the apoptotic cell, and (2) the β2-integrin activation of Rac1 to stimulate phagocytosis and activate the NADPH complex that generates reactive oxygen species to activate latent TGF-β. Active TGF-β, in turn, coordinates a response within the microenvironment by acting on multiple cells, including macrophages, myofibroblasts, and endothelial cells that control wound healing.