We previously reported that ORM was significantly elevated in the sera, liver and muscle tissues of fatigued rodents (for example, sleep-deprivation, forced swimming and treadmill-running models) and the sera of chronic fatigue syndrome patients.2, 24 Further studies demonstrated that ORM functioned as an anti-fatigue protein via activation of muscle CCR5 (C-C chemokine receptor type 5) to increase glycogen storage and muscle endurance.2 Therefore, we examined whether ORM participated in the differential regulation of fatigue and muscle endurance in males and females. Here, CCR5 is linked to myalgic encephalomeyelitis/chronic fatigue syndrome.