The ttw mouse is the most commonly used animal model for OPLL.3,10,48 The ttw mice exhibit increased angiogenesis40,60 and spontaneous ossification of soft tissues due to the loss of enpp1 inhibition of calcium and phosphorus deposition, which includes the posterior longitudinal ligament.48 While some studies have suggested that enpp1 gene polymorphism may be related to the pathogenesis of OPLL,61,62 the phenotype of OPLL patients is not completely identical to that of ttw mice resulting from enpp1 gene deficiency. The gene discussed is ENPP1; the disease is ossification of the posterior longitudinal ligament of the spine.