 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.  The authors\' measure number of cells with invadopodia (eg. [Figure 0B](#fig0){ref-type="fig"}), yet often conclude that cells have more invadopodia. If the authors are going to conclude that there are more invadopodia per cell, this is something that must be explicitly measured.  Importantly, the strikingly counterintuitive conclusion that increasing invadopodia inhibits invasion was not sufficiently justified. It remains a possibility that another pathway mediated by p00 is responsible for the invasion phenotype. One way to address this possibility would be to show expression of p00 0-000 is unable to rescue cell invasion.  It is not clear if the migration defect resulting from loss of p00Kip (Besson et al., 0000), is mechanistically distinct from the invasion phenotype reported here. In their previous publication, it was shown that inhibition of Rho kinase rescued migration. Does Rho kinase inhibition also restore the ability of the p00 -/- cells to invade through thin collagen layers? If not, it would strengthen the conclusion that the authors are investigating a novel migration mechanism downstream of p00^kip0^.  \[Editors' note: what now follows is the decision letter after the authors submitted for further consideration.\]  Thank you for resubmitting your work entitled \"p00^Kip0^ promotes invadopodia turnover and invasion through the regulation of the PAK0/Cortactin pathway\" for further consideration at *eLife*. Your revised article has been favorably evaluated by Fiona Watt (Senior editor) and 