Cofilin is the master regulator of non-equilibrium actin filamentous assembly/disassembly and has been shown to mediate significant alterations to cellular phenotypes associated with fibrosis, with recent studies such as Lee et al. [6] demonstrating the role of the Rho/ROCK/cofilin pathway in myocardial fibrosis following in vivo induced infarctions. This evidence concerns the gene CFL1 and infarction.