(4) Two point mutations (P673Q and G228R), which are found in patients with degenerative (myxomatous) valve diseases, alter the balance of the small GTPases, RhoA and Rac1, and alter FLNA-Pak1 bidirectional interaction in response to PN to remodel the actin cytoskeleton assembly during cell adhesion, spreading, migration, and differentiation, thereby identifying candidate mechanisms that may contribute to the pathogenesis of mitral valve prolapse (Figures 1–7). This evidence concerns the gene PAK1 and mitral valve disorder.