This pathway included A2M, PLAT and PLAU as STAT3-upregulated genes [45, 46] (the upregulation of these genes was confirmed by qRT-PCR, Supplementary Fig. S11), suggesting that STAT3 may also mediate the modulation by EML4-ALK of blood coagulation, which may have clinical implications in increased risk of disseminated intravenous coagulation in patients with EML4-ALK-positive cancer [47]. The gene discussed is EML4; the disease is cancer.