To elucidate the mechanism of heightened cell migration in FECD, we explored the drive for cellular cytoskeleton assembly in both normal and FECD cell lines and detected that FECD cells exhibit the higher activation of Rac1 compared to normal cells at baseline; however, these findings were further enhanced with the use of the RhoA inhibitor. This evidence concerns the gene RHOA and Fuchs endothelial corneal dystrophy.