Wound healing is a complex multistep process that involves a number of different cell types and requires tight regulation of biochemical and biomechanical signalling (1). Fibroblasts are required to deposit and remodel extracellular matrix (ECM) within the wound to provide mechanical stability and a protein scaffold for other cells and growth factors. This is achieved by their concerted migration to the site of injury initiated by chemoattractants that are secreted as a consequence of an inflammatory response. At the wound site, they are activated to convert into myofibroblasts that are able to exert strong forces to the underlying ECM resulting in its rearrangement and remodelling (1) (Fig. 1a).Importantly, fibroblast activation and the resulting matrix production need to be transient and reversible. Failure to terminate these processes leads to formation of keloids that are characterized by a thickened epidermis, increased number of mesenchymal cells as well as increased vascularization (2). Although the molecular mechanisms of keloid formation are not completely clear, keloid fibroblasts (KF) are assumed to play a critical role in the pathogenesis. KFs differ from normal fibroblasts in terms of production of cytokines and ECM components (2). However, their mechanical properties, which could influence the characteristic migratory properties as well as the ability to remodel the ECM (3), have not been addressed so far. Recently, Harn and co-workers have investigated the mechanical properties of KFs and the underlying changes in the cytoskeleton of these cells (4).Harn and co-workers discover that KFs bear a characteristic elastic behaviour that is mainly dominated by the actin cytoskeleton. Interestingly, filament elasticity of KFs displays a biphasic distribution. Areas of high and low elasticity are interpreted as assembling and disassembling focal adhesion sites, respectively. The authors show that coupling of mechanical forces of KFs to the ECM differs from normal fibroblasts in terms of strength and spatial distribution (4). The increased migratory behaviour of KFs is accompanied by an increased net force exerted to the substrate facilitating cellular movement via a mesenchymal-like mode of migration (Fig. 1b).We agree with the authors that the elastic behaviour of actin filaments is likely to mirror the magnitude of the force loaded on the filaments and the matrix and therefore influences cellular locomotion. We and others have observed similar behaviour in fibroblasts deficient in the integrin adaptor, integrin-linked kinase (ILK). These cells are unable to establish a stable link between ECM-bound integrins and the actin cytoskeleton and therefore display a disorganized actin cytoskeleton, a decline in traction force and a concomitant lower migration rate as well as a severe impairment in ECM remodelling (5). This highlights the importance of proper force transmission from the actin cytoskeleton to the ECM in fibroblast function.In line with this, Harn et al. (4) observed that inhibiting the activity of...