PAK2 and carcinoma: The neovascularization changes that we observe in slightly older PAK1−/− mice are potentially due to several of the abovementioned factors exacerbated by the absence of PAK1, not only in endothelial cells but also in auxiliary cells such as smooth muscle cells, fibroblasts and immune cells where PAK1 might be indispensable and where PAK2 cannot substitute for its function Interestingly, PAK1 and PAK2 appear to participate in distinct signaling cascades and in some cases play opposing roles in mast [74], breast [75], and prostate [76] carcinoma cells.