Double strand breaks (DBSs) promote multiple repair pathways and can give rise to different mutagenic processes. The propensity for activation directly affects genomic instability, with implications across health and evolution. However, the relative contribution of these mechanisms, their interplay and regulatory interactions remain to be fully elucidated. Here we present a new method to model the combined activation of non-homologous end joining, homologous recombination and alternative end joining. We use Bayesian statistics to integrate eight biological data sets of DSB repair curves under varying genetic knockouts. Analysis of the model suggests that in wild type and mutants there are at least three disjoint modes of repair. A density weighted integral is used to sum the predicted number of breaks processed by each mechanism, from which we quantify the proportions of DSBs repaired by each. Further analysis suggests that the ratio between slow and intermediate repair depends on the presence or absence of DNAPKcs and Ku70. We outline how all these predictions can be directly tested using imaging and sequencing techniques. Most importantly of all, our approach is the first step towards providing a unifying theoretical framework for the dynamics of DNA repair processes.