In the rotenone lesion model of PD, changes in the rhythmic expression of clock genes in the SCN, such as a phase delay in bmal1 or a phase advance in per1 expression (Mattam & Jagota, 2015), and lower amplitude of locomotor and body temperature rhythms and greater rhythm fragmentation (Lax et al., 2012) suggest a level of circadian rhythm dysfunction that may be of functional significance in the overall phenotype of the model. This evidence concerns the gene PER1 and Parkinson disease.