How are tumors with high MYB expression populated by TAMs, whether their recruitment, or proliferation is altered by tumor-derived cytokine network under control of c-Myb, whether such milieu could be mimicked by gene depletion/overexpression or pharmacologically, and how TAMs differ in their properties (not only quantity) in Myb-high vs. Myb-low tumors etc. should be investigated in preclinical models. The gene discussed is MYB; the disease is neoplasm.