A recent collaboration with the Roberts lab has been published in NAR Cancer [https://academic.oup.com/narcancer/article/5/4/zcad058/7479285], revealing that disruption of the cell’s ubiquitin-proteasome system, achieved through FDA-approved drugs for cancer treatment, elevates APOBEC3A levels in breast cancer and multiple myeloma cells. APOBEC3A, known for its role as a cytidine deaminase, is associated with APOBEC-induced mutations observed across various cancer types, contributing to genetic heterogeneity, tumor evolution, and adaptability. Our findings suggest that proteasome dysfunction, whether occurring naturally during cancer development or induced therapeutically, may enhance mutagenesis in cancer cells, potentially influencing therapeutic responses in patients. Congratulations Marina!