 describe a new mechanism, where p00 promotes Cortactin phosphorylation by Pak0 to reduce invadopodia and increase cell invasion through collagen. While the authors include a strong set of experiments that convincingly demonstrates a p00/Cortactin/PAK0 pathway exists, the manuscript overall feels somewhat preliminary because it is not clear how inhibition of this pathway can increase invadopodia formation and prevent cell invasion. Presenting a mechanism to explain this puzzling observation and more clearly demonstrating p00 is localized to matrix degrading structures would strengthen the novel, and important conclusions made by the authors. Additional concerns are listed below.  Major Concerns:  The pre-fixation permeabilization/extraction of the cytoplasm prior to staining for p00 does not give a lot of confidence that p00 is localized to invadopodia (as in [Figure 0A](#fig0){ref-type="fig"}, for example). Additionally, the Cortactin phosphomimetic construct decreases the number of invadopodia without significantly reducing the area of gelatin degradation, raising the strong possibility that the structures being identified by Cortactin (eg. [Figure 0A](#fig0){ref-type="fig"}) are not actual invadopodia, despite their punctate appearance. To make confirm these structures are invadopodia, the authors should show p00 is enriched in Cortactin or Tsk0 positive puncta which coincide with regions of matrix degradation.  