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We show that while a re-polarisation of the phenotype of macrophages, as considered by many recent experimental studies, can lead to tumour control, for tumour elimination it is required that macrophages are fully functional (i.e., the rate at which they kill tumour cells is high). We also show that a mixed macrophage's phenotype can keep the tumour under control in a state of dormancy. Moreover, an increase in this mixed phenotype can cause a delay in tumour reduction (accompanied by a larger tumour reduction), as well as a delay in tu
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