Exposure to ionising radiation is clearly associated with an increased risk of developing some types of cancer. However, the contribution of non-targeted effects to cancer development after exposure to ionising radiation is far less clear. The currently used cancer risk model by the international radiation protection community states that any increase in radiation exposure proportionately increases the risk of developing cancer. However, this stochastic cancer risk model does not take into account any contribution from non-targeted effects. Nor does it consider the possibility of a bystander mechanism in the induction of genomic instability. This paper reviews the available evidence to date for a possible role for non-targeted effects to contribute to cancer development after exposure to ionising radiation. An evolution in the understanding of the mechanisms driving non-targeted effects after exposure to ionising radiation is critical to determine the true contribution of non-targeted effects on the risk of developing cancer. Such an evolution will likely only be achievable through coordinated multidisciplinary teams combining several fields of study including: genomics, proteomics, cell biology, molecular epidemiology, and traditional epidemiology.