According to the two process model, sleep timing and duration are determined by the interaction of process S (the sleep homeostat) and process C (the circadian drive for alertness). Although originally invoked to account only for sleep inertia effects (post-awakening performance deficits), there is evidence that process W is also active during sleep, and that it serves a sleep-preserving function that is partly independent of processes S and C. This suggests that initiation of the natural, spontaneous awakening process at the end of an adequately restorative sleep period is not passively triggered by the combined effects of a reduced process S and an ascendant process C alone – it also requires that a process W-mediated barrier against awakening be breached. It is hypothesized that one function of REM sleep is to periodically test the level of stimulation needed to breach this barrier, with the extent to which cortical reactivation occurs during REM sleep reflecting the brain's level of sleep satiation. It is further hypothesized that this REM-elicited neuronal reactivation information is processed (possibly in the medial prefrontal cortex) to determine readiness for awakening, and this information is communicated (e.g., via the lateral hypothalamus) to the REM/NREM and sleep/wake “flip-flop” switches that either initiate awakening or the return to NREM sleep, as appropriate.