about the "progressive nature" of early-onset disease was not shared by Evers who argued in an Editorial that in the seven published trials where laparoscopy was performed before and after a period without treatment, in 71% of the cases the disease did not progress (2). Two considerations are in order when analyzing Evers' conclusion. On the one hand, it is clearly impossible to predict in which cases endometriosis will progress; on the other, the investigations upon which Evers based his conclusions were conducted in adult women and, over the last few years, we have argued that there is strong indirect evidence that the adult and the pre-pubertal and adolescent variants of endometriosis may have a different origin and phenotype (3). According to this hypothesis, early-onset disease traces its roots in the retrograde fetal endometrial shedding occurring in approximately 5% of neonates at the time of birth that is manifested by a well-documented, but neglected phenomenon called "neonatal menstruation" (4, 5). The visible bleeding with retrograde endometrial shedding has the ability to affect pelvic organs and become the source of disorders that may develop later in life and pose a risk for the future reproductive health of the adolescent (3, 6-8). We believe that the theory of a different origin of pre-pubertal or adolescent and adult forms of endometriosis is well founded, thanks to a series of investigations carried out half a century ago. At the