The increase in γ-H2AX phosphorylated at Ser139 (Figure 4B) by protein kinase ATM (mutated in ataxia-telangiectasia) leads to the recruitment of the mediator of DNA damage checkpoint protein 1 (MDC1) as a response to the formation of double strand breaks (DSB). Here, MDC1 is linked to Ataxia-telangiectasia.