Given our finding that USP1 is highly abundant in the WT Eμ-Myc lymphoma cells (Figure 5C, Supplementary Figure S6B), together with our data suggesting that USP1 can control CHK1 proteasomal degradation, we hypothesised that targeting USP1 might represent a viable therapeutic strategy in tumours with high levels of genomic instability and replication stress. The gene discussed is USP1; the disease is lymphoma.