We confirmed these results by overexpressing the chimeric POT1a/b and hPOT1 constructs in independently generated Pot1b−/−; p53−/− sarcomas, demonstrating that POT1ba and hPOT1 repress γ-H2AX TIFs to nearly undetectable levels (Supplementary Figure S6e–g). Here, H2AX is linked to sarcoma.