Further, PAK1-regulated tumor growth is either dependent on classical cell cycle regulation (the phosphorylation of Histone H3 [152] and the depolymerization of α/β-tubulin [153]) or anchorage-independent growth (the activation of MAPK or phosphorylated LC8 (dynein light chain) [154,155]), or it is depend on cell survival (phosphorylated FKHR (forkhead transcription factor) [156], DLC1 and BimL [157]). This evidence concerns the gene PAK1 and neoplasm.