Given that 2-h dinaciclib infusion had only transient effect on peripheral blast count, and given the observed pharmacokinetic and pharmacodynamic data, we performed in vitro studies on leukemia cells and demonstrated that prolonged exposures to dinaciclib (≥24 h), at concentrations (≤200 nM) that are far below the Cmax (>4,000 nM) observed in the clinical study, caused more profound and persistent down-regulation of Mcl-1 and/or p-Rb across all cell lines/primary leukemia cells, leading to more effective cell kill. The gene discussed is RB1; the disease is leukemia.