Using Siglec-F-depleting antibody to deplete eosinophils from established tumors and in PHIL mice, we also noticed that eosinophil deficiency enabled metastatic spread of a PDAC model with otherwise limited metastatic ability, implicating eosinophils as negative regulators of metastasis (Fig. 4k,l and Extended Data Fig. 3e–g); this prometastatic consequence of eosinophil deficiency was lost in the absence of cancer cell-derived ATX (Fig. 4m), consistent with a reciprocal interaction between eosinophils and ATX in the regulation of tumor progression. The gene discussed is ENPP2; the disease is cancer.