A role for circadian gene dysfunction has been established among the human sleep disorders, a subset of insomnias associated with circadian changes in the timing of sleep in humans [43], the most striking evidence for which is the familial advanced sleep-phase syndrome (ASPS) in which a phosphorylation site mutation of period homolog 2 (Drosophila) (PER2) was found to co-segregate with the disease in one extended family [44]. This evidence concerns the gene PER2 and insomnia measurement.