In the current study we have blocked formation of all 3-phosphoinositide species using the pan-specific PI3-kinase inhibitor wortmannin. As C. trachomatis inclusion recruitment of SNX- BAR proteins is not perturbed this indicates that the inclusion recruitment of SNX5 is likely driven by a protein-protein interaction (later shown to be IncE by SNX5 mutagenesis), rather than via 3- phosphoinositides including both the early and late-endosome enriched PtdIns3P and PtdIns(3,5)P2. We altered the text to emphasise wortmannin’s broad inhibitory effect to avoid confusion: “Interestingly, when infected cells are treated with wortmannin, a pan-specific inhibitor of phosphoinositide-3-kinase (PI3K) activity, we see a loss of the SNX proteins from punctate endosomes, but not from the inclusion membrane”. The reviewers suggest that we perform additional experiments using a specific inhibitor such as the Class III PI3K inhibitor Vps34-IN1, which will block specific formation of PtdIns3P. As wortmannin has no effect on inclusion recruitment, Vps34-IN1 is unlikely to provide additional insights.