Based on our results indicating (i) no difference in primary tumor growth between WT and EMCNecko mice (Fig. 2B) and that (ii) EMCN deficiency increased lung metastasis (Fig. 2F and I) and pulmonary vascular permeability (Fig. 3D), we hypothesized that EMCN deletion might contribute to enhanced colonization of metastatic cells after changes in the host microenvironment, which relies on the formation of a lung metastatic niche. Here, EMCN is linked to neoplasm.