This phenomenon is recognized as growth without growth hormone and may be related to a disordered GH-IGF-1 axis and hyperinsulinemia.[32,33] The delayed bone development may have been caused by GH deficiency, and the increase in body height during adulthood may be associated with hyperinsulinemia because of structural similarity between insulin and IGF-1 receptors.[33] In the biomechanical pathway of disease causation, obesity increases the shear stress across the epiphysis by reducing femoral anteversion,[34] and abnormal pelvic development is also an important risk factor for adult SCFE. Here, GH1 is linked to obesity due to melanocortin 4 receptor deficiency.