H2AX and B-cell non-Hodgkin lymphoma: As γH2AX foci accumulate at sites of V(D)J recombination in developing thymocytes [21], and a subgroup of T and B cell lymphomas in H2AX−/−p53−/−-deficient mice displayed oncogenic translocations arising as byproducts of aberrant V(D)J recombination, a role for H2AX in the process was hypothesized [65,66].