Centromeres are chromosomal regions that mediate kinetochore assembly and mitotic spindle binding; they are crucial to assuring faithful chromosome transmission during mitosis and meiosis. Centromeres might also play a role in chromosome condensation. In fact, depletion of the histone variant CENP-A, which defines centromere position, or its loading factor KNL-2 in C. elegans, leads to loss of centromere and kinetochore function, as well as chromosome condensation defects. However, the mechanism underlying these defects needs further investigation. Now, Florian A. Steiner and colleagues (Wenda et al., 2021) provide insight into the mechanism of how centromeres regulate the condensation of chromosomes. Using mass spectrometry and in vitro studies, the authors identify three residue targets for phosphorylation by CDK-1 in KNL-2, T750, S772 and S784. Moreover, in vivo studies in C. elegans reveal that mutation of these sites affects chromosome segregation and causes embryonic lethality. Interestingly, experiments with S772A/S784A mutants show that phosphorylation of these residues is not required for centromere formation and kinetochore assembly. However, reduced levels of condensin II on mitotic chromosomes and impaired chromosome condensation is observed in these mutant embryos. Taken together, these data uncover the direct contribution of KNL-2 in chromosome condensation in addition to its well-established role in centromere maintenance.