In this model, administration of TMP195 combined with anti‐PD1 antibody significantly suppresses tumour development, whereas a single treatment with TMP195 or anti‐PD1 antibody shows modest suppression of the tumour burden.47 Therefore, targeting master regulators of macrophage differentiation (e.g. MARCO, PI3Kγ and histone deacetylase) can be a potential approach to enhance checkpoint therapy by harnessing immune suppressive features and/or drawing antitumour functions in tumour‐infiltrating macrophages (Fig. 2c). The gene discussed is MARCO; the disease is neoplasm.