Instead, the role of Nek2 is to initiate the separation of centrosomes at G2/M by phosphorylation of two components of the intercentriolar linkage, rootletin and C-Nap1.4–6 Nek2 is overexpressed in several cancer cell lines and primary breast cancers and has been identified as a potential drug target in cholangiocarcinoma.7–10 Nek2 dimerizes through a C-terminal coiled-coil domain that is essential for efficient cellular activity11 and is activated by phosphorylation on its activation loop at T175, which is reversed by PP1-mediated dephosphorylation.12–14. This evidence concerns the gene NEK2 and cancer.