Human familial/idiopathic-type scoliosis (IS) is a complex genetic disorder for which the cause is unknown. The curve phenotype characteristically demonstrates pronounced morphological and developmental variability that is likely a consequence of biomechanical, environmental, and genetic differences between individuals. In addition, risk factors that affect the propensity for curves to progress to severity are unknown. Progress in understanding the fundamental biology of idiopathic-type scoliosis has been limited by the lack of a genetic/developmental animal model. Prior to consideration of teleosts, developmental idiopathic-type scoliosis has been considered to be exclusive to humans. Consequently, there is the notion that the syndrome is a result of bipedalism, and many studies try to explain the deformity from this anthrocentric viewpoint. This perspective has been reinforced by the choice of animals used for study, in that chickens and bipedal rats and mice demonstrate idiopathic-type curvature when made melatonin-deficient, but quadrupedal animals do not. Overlooked is the fact that teleosts also demonstrate similar curvature when made melatonin-deficient. Our characterization of the guppy curveback has demonstrated that non-induced idiopathic-type curvature is not exclusive to humans, nor bipedalism. We hypothesize that unique morphological, developmental and genetic parallels between the human and guppy syndromes are due to common molecular pathways involved in the etiopathogenesis of both phenotypes. We explore established gene conservation between human and teleost genomes that are in pathways hypothesized to be involved in the IS syndrome. We present non-induced vertebral wedging as a unique shared feature in IS and curveback that suggests a similar interaction between a molecular phenotype on the level of the vertebral anatomy, and biomechanics. We propose that rather than bipedalism per se, expression of idiopathic-type scoliosis is dependent on normal spinal loading applied along the cranio-caudal axis that interacts with an unknown factor causing the primary curve. In this regard, a comparative biological approach using a simplified teleost model will promote discovery of basic processes integral to idiopathic-type scoliosis in teleosts and humans, and highlight human-specific aspects of the deformity.