The notion that M-CSFR+ TIM, including both TAM and MO-MDSC-like cells, contribute significantly to tumor angiogenesis, was supported by Priceman et al. (115), showing that depletion of M-CSF-dependent TAM and MO-MDSC-like cells in the 3LL lung carcinoma model, using either the M-CSFR inhibitor GW2580 or a transgenic approach in chimeric mice, resulted in significant reduction in angiogenesis in TIM-ablated tumors (without a concomitant decrease in tumor growth). The gene discussed is CSF1R; the disease is lung carcinoma.