Moreover, considering the impaired activation of CHK1 but not CHK2 that we observed following SLF2 loss, the synergism of SUMOi with the highly specific CHK1 inhibitor rabusertib (King et al, 2014) was even more pronounced in OCI‐Ly1 and SU‐DHL‐4 cells, another intrinsically SUMOi‐resistant DLBCL cell line (Fig 8C). This evidence concerns the gene CHEK2 and diffuse large B-cell lymphoma.