Further evidence of the pro-tumorigenic cross-talk between sarcoma cells and TAMs was demonstrated in uterine LMS cells, where overexpression of maternal embryonic leucine zipper kinase (MELK), a serine/threonine kinase involved in cell cycle, apoptosis, and splicing regulation, contributed to doxorubicin chemoresistance both through an autonomous JAK2/STAT3 anti-apoptotic mechanism and through M2 macrophage polarisation via miR-34a/JAK2/STAT3. The gene discussed is MELK; the disease is sarcoma.