Wound closure and infection control are the primary goal of wound management. A variety of disinfectants and antimicrobial agents are widely available today and routinely achieve infection control. On the contrary, wound closure still remains a challenging goal. Cell adhesion, migration and contraction play significant roles in creating contractile force of patent wound margins and in contributing to wound closure. Modulations of these cellular behaviors have been investigated in the context of wound contraction; however, therapeutic strategy to achieve wound closure has not been established. Recently, we have reported that a previously unknown cytoskeleton molecule, wound inducible transcript-3.0 (wit3.0) also known as fibroblast growth factor receptor 1 oncogene partner 2 (FGFR1OP2), can significantly modulate fibroblast-driven wound closure in vitro and in vivo. The dynamic role of cytoskeleton in different experimental models may provide a novel platform for designing the therapeutic target of wound management.