We discovered risk sleepiness variants at 10 loci (e.g. PLCL1 and KSR2) and their GRS that associated with sleep propensity traits (higher sleep efficiency, longer sleep duration, fewer discrete sleep bouts, and fewer insomnia symptoms); whereas sleepiness variants at 27 loci (e.g. LMOD1, HCRTR2, and GABRA2, known to play a central role in sleep/wake control and narcolepsy57) and their GRS were more likely to contribute to sleep fragmentation (lower sleep efficiency, shorter sleep duration, more sleep bouts and more insomnia symptoms). The gene discussed is HCRTR2; the disease is insomnia measurement.