A prototypical example is that the exceptionally large coverings in prostate cancer may be due to the absence of data on gene fusions; in fact, over a half of the tumors could be accounted for by a small subset of such alterations (e.g., the fusion between TMPRSS2 and ERG, or other ETS family genes [55]). This evidence concerns the gene TMPRSS2 and Familial prostate cancer.