To test the function of CCR8 in anti‐tumour immunity, we measured the growth of subcutaneously implanted MC38 tumours in littermate WT and Ccr8−/− animals and compared this to the effect of systemic experimental ablation of Treg cells using Foxp3EGFP‐DTR mice, which express human diphtheria toxin receptor (DTR) and enhanced green fluorescent protein (EGFP) under the transcriptional control of the endogenous Foxp3 gene, enabling selective depletion of Foxp3+ Treg cells through administration of diphtheria toxin (DTx) [36]. Here, FOXP3 is linked to neoplasm.