Connolly and coworkers [20] demonstrated that radiotherapy stimulates increased production CCL2 and CCL5 at the tumour site, while Kalbasi and colleagues [21] found that ablative radiotherapy for pancreatic ductal adenocarcinoma led to a significant increase in CCL2 production by tumour cells, with genetic deletion of CCL2 in pancreatic ductal adenocarcinoma cells improving radiotherapy efficacy. Here, CCL5 is linked to pancreatic ductal adenocarcinoma.