The current model of cell cycle control features a succession of active cyclin-CDK (cyclin-dependent kinase) complexes, where accumulation of each successive cyclin leads to activation of its associated kinase. Cell fusion experiments have shown that nuclei sharing common cytoplasm progress through the cell cycle in synchrony. During schizogony of Plasmodium falciparum, nuclear division occurs asynchronously, and thus cannot be regulated by synthesis and accumulation of cyclins in the cytoplasm. We suggest that schizonts must have a ready pool of cyclins for activating all stages of the cycle, and that the cell cycle is regulated independently in each nucleus.