H2AX and cancer: Collis et al. were able to show in cancer cell lines that low-dose rate IR (i.e., 450 times lower than a high-dose rate producing environ 4–5 DSB/h instead of 1800 DSB/h) increased cell killing (clonogenicity) as a consequence of inefficient activation of the DNA damage sensor ATM and H2AX phosphorylation [365].