The hematopoietic cell-specific Rho GTPase-activating protein (GAP) ARHGAP19 acts on the RhoA and ROCK pathway during lymphocyte mitosis to mediate cell shape changes. Jacques Bertoglio, Muriel David and colleagues have previously provided evidence that ARHGAP19 is subject to post-translational modification, but the kinases responsible were unknown. In this study (Marceaux et al.), the authors now report that ARHGAP19 is sequentially phosphorylated by ROCK on S422, and on T404 and T476 by cyclin-dependent kinase 1 (CDK1), the major mitotic kinase organising cytokinesis. As shown here, ROCK-mediated phosphorylation of ARHGAP19 occurs in the nucleus before the onset of mitosis and enables its interaction with the 14-3-3 family of scaffolding proteins. CDK1 then phosphorylates ARHGAP19 in the cytoplasm after nuclear breakdown. Interestingly, interaction with 14-3-3 protects ARHGAP19 from dephosphorylation and so prevents its relocalisation to the plasma membrane, which would lead to untimely downregulation of RhoA activity during cytokinesis. This was confirmed in ARHGAP19 variants with mutated phosphorylation sites, which result in cytokinesis failure and multinucleated cells. Taken together, the findings presented here point to new regulatory pathways involving ROCK- and CDK1-mediated phosphorylation of ARHGAP19 and its interaction with 14-3-3 proteins for the timing of RhoA activation at late stages of mitosis.