FIGNL2 is a microtubule-severing enzyme that negatively regulates cell migration and wound healing. The protein localizes to the cell leading edge where it severs dynamic microtubules, thereby suppressing cell motility 1. Mechanistically, microtubule severing releases ARHGEF2, which activates RHOA to regulate focal adhesion turnover and suppress cell migration 2. FIGNL2 also functions as a negative regulator of axon regeneration by selectively severing dynamic microtubules in the distal axon and growth cone, and contributes to proper cell branching during endothelial and neuronal development. FIGNL2 is specific to vertebrates and shows notably reduced expression in the mammalian nervous system compared to lower vertebrates, reflecting its recent evolutionary origin 3. Clinically, depletion of FIGNL2 in mammalian cells increases the rate of cell movement more than twofold. Nanoparticle-encapsulated siRNA targeting FIGNL2 applied topically to murine excisional and burn wounds significantly enhances the rate and quality of wound closure, identifying FIGNL2 as a therapeutic target for cutaneous wound regeneration 1. A genome-wide interaction study identified an association between a FIGNL2 variant and elevated blood pressure in long sleepers 4.