In Eμ-MYC-driven B-cell lymphomas, for example, perturbation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway through loss of cellular homolog of the viral oncogene Rel (cREL) or mutation of RELA proto-oncogene, NF-kB subunit (RELA) (T505A) leads to CHK1 inhibitor resistance, either by complete loss of CHK1 protein, driven by ubiquitin carboxyl-terminal hydrolase 1 (USP1) down-regulation, or by reduced CHK1 activity due to diminished CLASPIN expression. This evidence concerns the gene USP1 and B-cell non-Hodgkin lymphoma.