Dear Editor, We read with interest the comment of Dietz [1] about our review article on the biochemical, biomolecular and genetic basis of pelvic organ prolapse (POP) [2]. Besides presenting an overview of the literature, our objective was to provide the readers with a critical analysis of the recent studies in this field including a detailed discussion of the methodology, but not of the etiology of POP. We, however, totally agree that pelvic floor trauma caused by childbirth is the major risk factor for the development of pelvic floor dysfunction [3], as mentioned in our introduction [2]. Our conclusion regarding “... the most important causes of variations are still unknown...” refers to the individual genetic variations, and not to the causes of POP, thus highlighting the need for additional and large-scale genomic investigations. It is very likely that the genetic component plays a role in the pathogenesis of POP, as suggested by many epidemiological, family-based and linkage, expression and candidate gene association studies [4–11]. Our conclusion, therefore, relies on a basic biological principle: the final phenotype is the result of interaction between the individual genotype and environmental factors. Since the latter is most probably vaginal delivery in the case of POP, we should endeavor to find out more about the genotypic variations in the future. Animal models of POP, including genetic models, allow testing the mechanistic relationship between cause and effect of POP initiators by limiting the number of studied variables [12–14]. In contrast, clinical studies, by their nature, are never perfectly controlled. The problem is also aggravated when dealing with a dysfunction of multifactorial etiology as POP. This point was already addressed throughout the manuscript [2]. The biomolecular and biochemical analysis of pelvic floor tissues in women provides a golden opportunity for detecting a number of proteins and genes that are over-expressed and/or under-expressed in patients with POP versus controls. Those studies enable us to better discern the complex interplay between pelvic floor structural composition and support capacity. Although the mechanisms by which different risk factors in women including childbirth trauma lead to POP may be different, evidence suggests that all share a final common pathway involving a dysregulation in synthesis and/or assembly or degradation of the molecular components of the pelvic floor supportive tissue [15–18]. Human studies can further contribute to this field by offering some clues for the molecular etiology of POP thus providing a platform for further investigation of specific gene targets. In this context, genetic screening is the next obvious step required for understanding POP predisposition and its molecular basis. Sir William Osler (1849–1919) previously recognized that “variability is the law of life, and as no two faces are the same, so no two bodies are alike, and no two individuals react alike and behave alike under the abnormal conditions we know as disease”. Personalized medicine has rapidly advanced the prediction of disease incidence as well as achieving the goal of “the right treatment to the right person at the right time” based on the individual’s clinical, genetic and environmental information [19, 20]. Genomic data is the driving force behind personalized medicine. Since M. A. Bortolini (*) Department of Gynecology, Federal University of Sao Paulo, Sao Paulo, SP, Brazil e-mail: maria.augusta@gmail.com