Combined knockdown of TK1/DCK in PCa cells induced a modest replication stress response (Figure 5A,B, Supplementary Figure S6A–C), and addition of the deoxynucleotide monophosphate (dNMP) products of TK1, DCK and TS activities dose-dependently recovered basal γH2AX levels in 5-FU-treated cells (Figure 5C). This evidence concerns the gene DCK and posterior cortical atrophy.