These observations are consistent with the known role of chromothripsis and chromoplexy in generating driver events or oncogenic gene fusions in multiple fusion-driven cancer types (including EML4-ALK in lung adenocarcinoma and TMPRSS2-ERG in prostate cancer)21,109,113,119,131,133,134,137,185,186, as well as having the potential to disrupt multiple drivers at once in a single catastrophic event. This evidence concerns the gene ERG and Familial prostate cancer.