Tumour associated macrophages (TAMs) are often the most abundant immune cell type in tumours where they support progression to invasion and metastasis. However, macrophages are highly responsive to local influences, which gives rise to subtypes of TAMs that differ in their pro- or anti-tumoural activities. Accordingly, therapies targeting all TAMs such as those targeting the CSF-1/CSF-1R axis have been disappointing and blocking pro-tumoural behaviour(s) may be a more effective approach. My laboratory is interested in how actively motile macrophages promote tumour invasion downstream of the CSF-1R. Using a mouse model of breast cancer, selective inhibition of two CSF-1 activated regulators of macrophage motility, Hck and PI3K p110δ, reduced tumour growth by up to 70%. We are currently investigating whether this response is due to TAM phenotype reprogramming or TAM motility inhibition and are also extending the approach to other cancer models.