Recent work by Redon et al. showed that growing tumors may act as a type of stress in the organism and induce complex DNA damage (DSBs and OCDLs) in distant proliferative tissues in vivo . According to this study, rapidly growing normal tissues, such as colon and skin were found to be particularly susceptible to remotely induced DNA damage and a signaling molecule involved in inflammation, the chemokine CCL2 (monocyte chemoattractant protein-1: MCP-1) appeared to be a major player in promoting this distant effect. Interestingly, later studies by the same groups showed that this systemic DNA damage accumulation under tumor growth can be inhibited by the antioxidant Tempol suggesting the involvement of oxidative stress . The involvement of CCL2 and macrophage activation in tumor-induced distant DNA damage suggests some resemblances with the chronic tissue stress responses usually referred to as para-inflammation , which relies mostly on alternatively activated macrophages (M2) rather than on classically activated macrophages (M1) associated with the acute inflammatory response .