I. IntroductionSleep is of fundamental importance in our daily lives. Prolonged sleep deprivation can cause a decline in the immune system and, in the worst case, death. As everyone can understand, our sleep-wake cycle is relatively regular and stable, and there is a reason for our regular biological cycles: the suprachiasmatic nucleus (SCN). In our body, multiple biological clocks regulate circadian rhythms such as the sleep-wake cycle and hormone release rhythms. Within the hypothalamus, the suprachiasmatic nucleus (SCN) contains the master clock that regulates peripheral circadian clocks in the brain from becoming out of sync with each other. The SCN also receives information from the retina for light entrainment and thus keeps the entire system in synchrony with the light-dark (LD) cycle. The central dogma in the field of circadian biology is that light is the primary zeitgeber, the signal that drives the circadian rhythm. Many studies show that diurnal neuronal activity of the SCN and light-induced neuronal activity of the SCN inhibit locomotor activity in nocturnal rodents. However, several studies demonstrate that anticipatory eating behavior (FAA), induced by limiting food to a few hours a day, can be zeitgebers that supersede all other cues, including light. Rodents can anticipate a predictable daily meal by entraining circadian oscillators. Studies show that this anticipatory behavior does not require the master circadian clock within the SCN and this has led to the hypothesis that there are food-introduced oscillators (FEOs) in the brain responsible for anticipatory behavior. However, the circadian oscillators responsible for FAA are still unknown. In this paper, I… halfway through the paper… may not seem practical, it may shed new light on the position of FEOs. Furthermore, further testing using different clock genes needs to be performed to determine whether DMH is truly involved in FAA or simply downstream of other circadian oscillators that drive FAA. If in reality there are multiple FEOs at play, as proposed by Feillet et al. (2008), then experiments that combine lesions at multiple sites are needed to produce FAA impairments (Feillet and Mendoza, 2007). Again, since the answer is open to infinite possibilities, I also participated in the research trying to locate FEOs. However, my results did not yield any significant rhythms in the DMH when we performed in situ hybridization targeting the clock gene Baml1. After reading these articles, perhaps a future research direction, for me too, will be to consider FEOs other than DMH.