XPR1-mediated phosphate export reduces platelet polyP content and thereby limits platelet-dependent FXII activation and thrombosis. In the absence of functional XPR1, phosphates are no longer exported, which results in increased polyP levels in dense granules of platelets. Consequently, at sites of platelet activation, more polyP is released, which results in increased thrombosis as demonstrated by Mailer et al. It will be interesting to further investigate whether elevated polyP levels as a consequence of reduced XPR1 activity would also translate into increased thromboinflammation and/or might reduce inflammatory bleeding. This figure was created using BioRender.com.