This paper describes a paradoxical relationship between the cell cycle transcription factor FoxM1 and a Cul4-based ubiquitin ligase. FoxM1 is recurrently activated in aggressive breast and ovarian cancers, and this study shows that VprBP, a substrate receptor for Cul4, controls both the degradation and activation of FoxM1. Moreover, we showed that VprBP is overexpressed in high-grade serous ovarian tumors, potentially contributing to FoxM1 activation in malignancy. This study was a collaborative efforts with our colleauges at UNC, in the Bowers and Bae-Jump labs. Read more here.