In a murine colon adenocarcinoma model, treatment with two mAbs to concomitantly block CSF‐1R and stimulate CD40 resulted in the reprogramming of TAMs by increasing pro‐inflammatory signals such as IL‐12B, IL‐27, IL‐1β and CCL5.44 In addition, in a melanoma tumor model, the depletion of CD163+ TAMs, using an anti‐CD163 antibody conjugated to a doxorubicin charged liposome, led to a monocyte influx, the up‐regulation of IFN‐related cytokines and an anti‐tumor T‐cell response.45 The gene discussed is CCL5; the disease is neoplasm.