Our data build upon previous preclinical (17, 39) and clinical studies of CDK inhibition in NB including studies of (a) dinaciclib, a broad spectrum, but poorly tolerated clinical inhibitor of CDKs (including CDK 1,2,5,9), which exhibited antiproliferative activity as a single agent and together with chemotherapy in NB cell lines and in vivo models; and (b) seliciclib (CYC202, R-roscovitine), an inhibitor of CDK2/5/7/9 that exhibited only partial activity against MYCN and was further limited by lack of potency and rapid clearance (19–23). Here, CDK2 is linked to neuroblastoma.