Recent advances in understanding the biomolecular mechanisms of sleep control in the Drosophila model have implicated mitochondrial ROS as a key cog in the machine. Hyperkinetic, the beta subunit to the potassium channel Shaker, has been shown to act as a conduit translating rising levels of that mitochondrial ROS during waking hours to heightened cell excitability in the sleep-controlling dorsal fan-shaped body-projecting neurons (dFB) in flies. In order to explore the universality of this mechanism, we instigated a parallel study in mice. Hyperkinetic has three homologs in the mammalian genome–Kcnab1, Kcnab2, and Kcnab3–which encodes the beta subunits to the voltage-gated potassium channel Kv1 family members. Interestingly, the proteins encoded by the genes, Kvβ1-3, have dual function in that on top of gating ion flow through Kv1 they also have a functional aldo-keto reductase (AKR) domain. The two functions are coupled, with the activity of the AKR determining the A-type inactivation (or lack thereof) imposed by the beta subunit on the channel. Having opted for a dual approach, one genomic deletion and the other a point mutation targeting the function of the AKR, we found that deletion of the beta subunits lead to reduction in sleep, whereas mutation targeting AKR function leads to consolidation of sleep. Close analysis of the sleep architecture points to changes in NREM to REM transition onset, with protein expression profile showing strong localization in relevant brain regions. These results suggest at least partial conservation of mechanism from the fly to the mouse.