H2AX and neoplasm: This hyperactivation of DNA-PK leads to downstream targets of phosphorylation, such as histone H2AX, leading to a pan-nuclear γH2AX signal.9 This false damage signalling inhibits the recognition of genomic DSBs and the recruitment of repair proteins for efficient repair.8,9 AsiDNA also acts as a lure for PARP1 proteins, which are also hyperactivated, leading to the sequestration of proteins acting in the same pathway (XRCC1, PCNA).10 This overall hyperactivation of DNA-PK and PARP proteins allows quantifying the activity of AsiDNA in cells and tumours.