Loss-of-function mutations of SH2B3/LNK in human carriers and LNK-deficient murine models promote eosinophilia and activate peripheral eosinophils via uncontrolled JAK/STAT signaling and downstream upregulation of surface receptors like CD11b and CD69. This activated eosinophil phenotype leads to degranulation and formation of oxidized phospholipids and promotes EET-osis. Eosinophil-released OxPLs promote neutrophil activation via PAFR-mediated signaling, leading to increased neutrophil recruitment and NET formation. Reciprocal eosinophil and neutrophil activations then culminate in a prothrombotic state, leading to atherothrombosis. Eosinophil depletion, pharmacological degradation of ETs by DNase I, or targeted approaches like inhibition of IL-5 may therefore serve as novel antithrombotic therapeutic concepts in eosinophil-driven diseases.