Consistent with the diverting effect on macrophage polarization in a breast cancer model in vivo [29], we showed that the treatment of TMP195, a selective class IIa histone deacetylase (HDAC) inhibitor, resulted in an increased number of CD11b+ macrophages within CRLM, as well as decreased PV F4/80+ TAMs and tumor vessel corruption. Here, HDAC9 is linked to breast cancer.