Wound contraction is associated with collagen organization. Is cell contraction or cell tractional forces responsible for collagen organization? Myofibroblasts (Mfibs) are identified by αSMA stained stress fibers. Fibroblast populated collagen lattice (FPCL) contraction can occur by cell contraction or tractional forces. FPCL cast under identical conditions are either released in 1 hour after manufacture, free‐floating (FF) FPCL or released on day 4, attached delayed released (ADR) FPCL. FF‐FPCL contraction, completed in 2 days in the absence of cell contraction, shows collagen organization but no αSMA staining. ADR‐FPCL contraction, completed in less than 2 hrs had αSMA stained contracted cells, but no collagen organization. Vanadate treated FF‐FPCL contract with collagen organization. Vanadate treated ADR‐FPCL showed impaired contraction, few αSMA stained contracted cells and no organized collagen. Apparently, ADR‐FPCL contraction requires αSMA contracting cells. At confluence almost all low density (LD) plated fibroblasts express αSMA. Vanadate or a native collagen blanket placed on confluent LD plated cells eliminates αSMA staining. With tension fibroblasts in collagen express αSMA. Without tension collagen eliminates αSMA expression. By day 7 open rat wounds close by 50% with organized collagen, but no Mfibs. Vanadate treated rat wounds close at the same rate as untreated wounds, but no Mfibs ever appear. At 3 wks the wall of the rat crotin oil granuloma is exclusively populated with Mfibs. Removal of aliquots of wound fluid daily for 3 days leads to granuloma compaction. Collagen fibers show increased organization and Mfibs are replaced by fibroblasts. It is proposed that Mfibs are associated with fibroblasts entering apoptosis. Death associated protein (DAP) kinases are a family of kinases that induce programmed cell death and phosphorylate myosin light chains (MLC). MLC phosphorylation leads to αSMA expression. The triggers for generating αSMA in stress fibers is tissue placed under tension and/or induced apoptosis through a DAP kinase. The functions of Mfibs are to counteract transient changes in tensions within granulation tissue and to prepare cells to enter apoptosis. Wound contraction advances by fibroblast organization of collagen in the absence of cell contraction.