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However, numerous observations have been at variance with this dogma. In the 1950s, attention was drawn to abscopal effects in areas of the body not directly irradiated. In the 1960s reports began appearing that plasma factors induced by irradiation could affect unirradiated cells, and since 1990 a growing literature has documented an increased rate of <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> damage in the progeny of irradiated cells many cell generations after the initial exposure (radiation\u2010induced genomic instability) and responses in non\u2010irradiated cells neighbouring irradiated cells (radiation\u2010induced bystander effects). All these studies have in common the induction of effects not in directly irradiated cells but in unirradiated cells as a consequence of intercellular signalling. Recently, it has become clear that all the various effects demonstrated <jats:italic>in vivo<\/jats:italic> may reflect an ongoing inflammatory response to the initial radiation\u2010induced injury that, in a genotype\u2010dependent manner, has the potential to contribute primary and\/or ongoing damage displaced in time and\/or space from the initial insult. Importantly, there is direct evidence that non\u2010steroidal anti\u2010inflammatory drug treatment reduces such damage <jats:italic>in vivo<\/jats:italic>. These new findings highlight the importance of tissue responses and indicate additional mechanisms of radiation action, including the likelihood that radiation effects are not restricted to the initiation stage of neoplastic diseases, but may also contribute to tumour promotion and progression. The various developments in understanding the responses to radiation exposures have implications not only for radiation pathology but also for therapeutic interventions. Copyright \u00a9 2013 Pathological Society of Great Britain and Ireland. 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