compensation is a key feature of ttfls that regulate circadian rhythms. bmal1 compensates for clock in that if clock is absent, bmal1 will upregulate to maintain the mammalian circadian rhythms. npas2 has been shown to be analogous to the function of clock in clock-deficient mice. in "clock" knockout mice, npas2 is upregulated to keep the rhythms intact. "npas2"-mutant mice, which do not express functional npas2 protein, still maintain robust circadian rhythms in locomotion. however, like clock-deficient mice in the clock/bmal1 ttfl, "npas2"-mutant mice (in the npas2/bmal1 ttfl) still have small defects in their circadian rhythms such as a shortened circadian period and an altered response to changes in the typical light-dark cycle. in addition, "npas2" knockout mice show sleep disturbances and have decreased expression of "mper2" in their forebrains. mice without functional alleles of both "clock" and "npas2" became arrhythmic once placed in constant darkness, suggesting that both genes have overlapping roles in maintaining circadian rhythms. in both wild-type and "clock" knockout mice, "npas2" expression is observed at the same levels, confirming that "npas2" plays a role in maintaining these rhythms in the absence of "clock".