Engagement of CCL5 with its receptor, C-C chemokine receptor type 5 (CCR5), can favour tumour growth by several mechanisms including induction of the mammalian target of rapamycin (mTOR) pathway,20,21 and by recruiting tumour associated macrophages (TAMs), leading to immunosuppression and release of pro-angiogenic cytokines.22,23 The CCL5-CCR5 axis has also been implicated in tumour migration and metastasis through modulating the activity of the PI3K/Akt, MAPK/ERK and NF-ĸB pathways, and via induction of matrix metalloproteinases.24 The gene discussed is AKT1; the disease is neoplasm.