Breast Cancer (BC) is one of the most common forms of cancer and accounts for 6.9% of cancer deaths. BC is a highly complex and heterogenous disease, with each individual tumour displaying unique molecular and behavioural characteristics. Lemur tyrosine kinase 3 (LMTK3) is a key component in the oncogenic pathways involved in a multitude of cancers, including subtypes of BC. Tumours displaying LMTK3 overexpression are associated with higher cancer aggressiveness, invasion, drug resistance, and overall poor clinical outcomes. Extracellular vesicles (EVs) are small, lipid enclosed packages released from cells that can assist in cell-to-cell communication. Messages are transferred using the lipids, proteins, and nucleic acids contained within. Cancerous cells release EVs to aid in cancer crosstalk and establish the tumour microenvironment through influencing surrounding cells, including immune cells, to promote tumour growth. Our research shows that LMTK3 overexpressing BC cells release EVs increased in size and with altered cargo in comparison to wildtype BC EVs. These LMTK3 EVs are then taken up by monocytes (a type of immune cell). After being treated with LMTK3 EVs, the monocytes had a reduced ability to migrate, as well as a reduced invasion into 3D BC cell spheres.