In mouse models of spontaneous breast cancer metastasis, upregulation of IL-33 in metastases-associated fibroblasts instigated type 2 inflammation in the metastatic microenvironment and mediated recruitment of eosinophils, neutrophils, and inflammatory monocytes to lung metastases, further indicating a pivotal role of IL-33 expressing CAF in establishing a hospitable inflammatory niche in lung metastases [91]. The gene discussed is IL33; the disease is breast carcinoma.