We show that tumor-educated Gr1+CD11b+ (Tu-Gr1+CD11b+) cells, rather than Gr1+CD11b+ cells from spleen (Spl-Gr1+CD11b+) or bone marrow (BM-Gr1+CD11b+) from tumor-bearing mice, effectively modulate tumor plasticity via OSM/IL-6/JAK signaling by rapidly and transiently converting SCA1– cells into SCA1+ cells with high metastatic capacity. The gene discussed is IL6; the disease is neoplasm.