Observation of an absence of a bystander effect in the present study may help explain the sensitivity of radioresistant tumor cells to neutrons, because there is a possibility that the protection otherwise provided by the bystander effect on the tumor in response to neutrons is absent or not strong enough in magnitude, thereby causing tumor cells to be killed. The risks currently associated with neutron exposure may be over or underestimated depending on which model of risk estimation is used to predict low dose risks from high dose data. Hence, reevaluation of radiation protection standards may be required. The work described in this paper may be relevant for radiation oncologists planning cancer treatments that involve fast neutron or proton radiotherapy, particularly for pediatric patients or pregnant women. This study used cells that lack gap junctions. There is a possibility that a neutron-induced bystander effect requires physical contact between cells, which could be tested by performing experiments using cell lines such as fibroblasts and keratinocytes that have gap junctions. If no bystander effect is induced in these cell lines, then it may be likely that neutrons do not have any ability to induce a bystander effect. Another possible explanation for the lack of a bystander effect with neutrons observed in this study may be the presence of dimethyl sulfoxide, a scavenger of reactive oxygen species, which was used to dissolve cytochalasin B that is required for the cytokinesis-block micronucleus assay. Both pre- and post-radiation treatment with DMSO is known to suppress DNA damage in irradiated cells. However, this possibility seems unlikely in the work described here because we observed a bystander effect with an identical procedure involving DMSO when the same cell lines were exposed to photons. However, if a very small bystander effect was in fact induced by neutrons, then it may have been obscured by the DMSO, whereas the bystander effect induced by high levels of photons was too large to be masked by DMSO. For cells irradiated with high doses of photons, a considerable amount of damage was attributed to the bystander component. The percent contribution by the bystander exposure to the direct exposure was highest at the lowest dose delivered and then it appears to saturate as dose increases, perhaps because there is saturation either of the bystander signals or the cellular responses to those signals. This observation is in agreement with other reports. For cells irradiated with neutrons there is little or no damage that can be attributed to a bystander effect, because as previously noted, there is comparatively less oxidative damage following neutron than gamma exposure. We report two RBEs for neutron radiation, one for micronuclei and the other for nucleoplasmic bridges. These two genetic endpoints have different mechanisms of formation.