We demonstrated that targeting the CSF1/CSF1R axis, which is implicated in macrophage differentiation and polarization towards an angiogenic and pro-tumor, M2 phenotype [29,30], using a CSF1R inhibitor (currently tested against advanced solid tumors, NCT02829723), can retard mouse mesothelioma growth in vivo without affecting tumor cell proliferation in vitro and hamper tumor angiogenesis though endothelial cells do not express its target receptor [30]. This evidence concerns the gene CSF1R and mesothelioma.