Sleep and wakefulness are controlled by specific brain regions. These regions have been identified by classical elimination of brain regions or by acute manipulation of neural activity. However, acute manipulation of these regions often has only a temporary effect on the sleep-wake cycles and chronic inhibition of neural activity in these areas has little effect. These may have been an adaptation and compensation by other brain regions. The preoptic area (POA) has long been recognized as the sleep center first proposed by von Economo. However, a recent optogenetic study found that photostimulation of POA GAL neurons at 10 Hz failed to increase sleep and surprisingly increased wake. These results call into question whether POA neurons promote sleep. This study investigated the effects of brain region-specific cell ablation and chemogenetic activation in the POA on the sleep-wake cycle. In this ablation method, we injected taCasp3 AAV, which overexpresses procaspase-3 in a Cre-dependent manner and induces apoptosis, in the POA-specific to avoid the effects of passing axons and ablate the cells in the brain region. The cell ablation results showed the fragmentation of the sleep-wake cycle. In addition, there was no longer a difference between light and dark periods. This effect was sustained for more than four weeks, and other brain regions were not compensated. Next, chemogenetic activation of POA by intraperitoneal injection of CNO (Clozapine-N-Oxide) surprisingly observed the fragmentation of the sleep-wake cycle. These results suggest that the POA may not be simply a sleep-promoting region, as previously reported.