Moreover, in accordance with recently reported findings showing that SPOP promotes the transcriptional expression of DNA repair factors including RAD51 and CHK1 and that SPOP knockdown impairs RAD51 foci formation and CHK1 activation at the transcriptional level in response to replication stress [14], we found that the expression of the two genes was markedly reduced at both RNA and protein levels in siSPOP-transfected PCa cells. The gene discussed is SPOP; the disease is posterior cortical atrophy.