In another in vivo study, adopting an AS-like mouse model (CD4-Cre;Ptpn11f/f) characterized by kyphosis, scoliosis, arthritis, and bony fusion of axial joints, the authors observed that targeting dysfunctional chondrogenesis with a Smo inhibitor significantly reduced the AS-like bone disease in mice [63]. This evidence concerns the gene SMO and arthritic joint disease.