Furthermore we have identified the CX3CR1 ligand fractalkine as a key driver of NK cell migration to soluble factors in the OAC omentum, but not tumour, presenting CX3CR1 antagonism as an attractive therapeutic approach to impede erroneous NK cell recruitment to the omentum and concurrently, maximise their availability to traffic to the tumour in obese cancer patients [12]. This evidence concerns the gene CX3CR1 and neoplasm.