Ataxin-3L binds to KLF5, and remove the ubiquitin chains on KLF5, thus preventing its degradation. KLF5 functions as a transcriptional factor essential for the promotion of breast cell proliferation, survival, and tumorigenesis. According to this study, Ataxin-3L would antagonize ubiquitination and proteasome-mediated degradation of KLF5, which means this DUB’s inhibiting activity may be a potential therapeutic target for breast cancer intervention. (32982735)