TANs‐derived CXCL8 and IL17A trigger EMT by increasing expression of SNAIL, TWIST, and ZEB1, which reduces cell–cell contact;[35, 36] TANs‐secreted MMPs, serine proteases and cysteine cathepsins inhibit activation of NK cells and promote extravasation of circulating tumor cells;[37] Moreover, TANs facilitate survival and seeding of metastatic cells by remodeling the extracellular matrix (ECM) and build an immunosuppressive environment.[38]. The gene discussed is SNAI1; the disease is neoplasm.