CK1ε and CK1δ are essential in the genetic transcription-translation (and post-translation) feedback loops that generate circadian rhythm in mammals.
The previously-characterized CK1ε isoform was first implicated as a clock gene when its Drosophila homolog, double-time (Doubletime (gene)), was discovered in 1998. Double-time is 86% identical to human CK1ε. Kloss et al and Price et al showed that mutations in double-time altered circadian rhythm.  They found two DBT mutants that had abnormal free-running periods and one that was pupal-lethal but resulted in accumulations of hypophosphorylated PER protein.  Since then,  double-time's protein product DBT has been well characterized for its role in phosphorylating PER, the protein product of clock gene period in Drosophila, and its mammalian homologs appear to play a similar role.
In 2021, scientists reported the development of a light-responsive days-lasting modulator of circadian rhythms of tissues via Ck1 inhibition. Such modulators may be useful for chronobiology research and repair of organs that are "out of sync".