 In IVF cycles, poor responders often develop a dominant follicle and multiple small follicles rather than multiple large follicles which is the goal of such treatment. In such cases, the IVF cycle is often cancelled. The physiology behind such asynchronous follicular growth during COH is poorly understood. Such discrepant growth may be the result of size differences in early antral follicles 8. It is also possible that the premature FSH elevation that occurs in the late luteal phase of the menstrual cycle plays a role in this process 9. FSH prevents follicular atresia at the end of the luteal phase10. Some follicles are intrinsically more sensitive to FSH and able to respond to low levels of this hormone than others. Given the fact that larger follicles are often more FSH-responsive than small follicles, it makes sense that exogenous gonadotropins may lead to worsening follicular asynchrony during COH 11. 