To rule out the possibility that the resistance of p65EKO mice to tumour development could be a consequence of impaired DMBA metabolism, we investigated DNA damage responses (DDR) in the epidermis of p65EKO and control mice by examining the phosphorylation of histone H2AX, γH2AX, which is generated in the vicinity of DNA damage lesions (Lukas et al, 2011). This evidence concerns the gene H2AX and neoplasm.