SPOP mutations represent a distinct subclass of PCa, in that tumors with SPOP mutations generally lack other common features of PCa, including the PCa-specific TMPRSS2 and ETS family gene rearrangements (present in ~50% of PCa), abnormalities in the phosphatidylinositide 3-kinase pathway, or deletion and mutations of the tumor suppressor gene TP53 [2, 4–6]. This evidence concerns the gene TMPRSS2 and posterior cortical atrophy.