Cancer cells frequently co-opt functions of healthy cells and tissues. During metastasis, circulating tumour cells (CTCs) escape into new tissues through extravasation. Thrombosis is positively correlated with metastasis, suggesting that CTCs might usurp the clotting process to promote extravasation. In this Short Report (Ward and Martin, 2023), Juma Ward and Paul Martin use zebrafish larvae to visualise interactions of blood clots, thrombocytes (zebrafish platelets) and immune cells with engrafted CTCs. CTCs quickly become associated with fibrin and also preferentially localise to laser-induced microclots. Treatment with the anticoagulant warfarin reduces both clotting and extravasation, supporting the role of clots as a pre-metastatic niche. Correlative light and electron microscopy (CLEM) of microclots reveals close interactions of CTCs with macrophages and neutrophils, and the authors find that blocking immune cell recruitment to clot-associated CTCs significantly reduces the incidence of extravasation. Interestingly, the recruited macrophages show an anti-inflammatory phenotype. Treatments that induce a pro-inflammatory switch in macrophages, including knockdown of fibrinogen, tend to suppress extravasation, suggesting that CTCs co-opt the clotting response to attract ‘friendly’ immune cells that protect them, facilitate migration and even support angiogenesis. Taken together, these findings help explain the antitumour effect of warfarin and mechanistically link thrombosis with metastasis.