I am a board-certified pediatric urologist and a scientist-surgeon working at Nemours Children's Health Florida with a clinical and research focus to study and understand molecular mechanisms that if altered, lead to genitourinary (GU) birth defects. I see and treat patients with such GU anomalies daily, yet it baffles me that we are only beginning to appreciate the complexity of molecules and pathways that direct the development of the GU tract towards normal or abnormal outcomes. Understandably, this is not an exclusive concern of physicians and scientists since patients legitimately wonder whether we actually know what causes these defects or how these defects can be treated and even prevented. It is precisely for these reasons that I became passionately engaged in bench research during my 3-year research intensive fellowship in pediatric urology at Boston Children’s Hospital in 2013. There, under the guidance of Dr. Rosalyn Adam and Dr. Joshua Mauney, I worked in the areas of bladder smooth muscle physiology and tissue regeneration, which led to five groundbreaking publications and several presentations at national meetings. In keeping with experience, I focused my urologic training on research opportunities to acquire the needed skills and knowledge to become a successful physician scientist in a research field coherent with my acumen and accrued expertise. I also successfully completed the Clinical Scientist Training Program at BCM, which is a program designed for academically motivated faculty to develop essential tools in conducting hypothesis-driven, patient-oriented research. In such capacity, I was recruited as the first surgeon-scientist in the Division of Urology at Texas Children’s Hospital (TCH)/Baylor College of Medicine (BCM) and worked as a K12 scholar for the last five years under the mentorship of Dr. Dolores Lamb, which led me to the discovery that dosage variations in KCTD13 and CUL3 genes, suspected to be critical to ubiquitination cascades, are prominently more common in patients with GU birth defects. Consistent with these findings, we hypothesize that KCTD13 and CUL3 genetic alterations could be major drivers of the pathogenesis of such diseases by directly or indirectly hindering normal GU development. I was awarded an R01 to study these mechanisms 4 years ago and have continue this work at Nemours Children's Health Orlando.