We generated non-inducible and inducible Runx1-deficient mice (Runx1f/fCol2α1-Cre and Runx1f/fCol2α1-CreER mice) and found that chondrocyte-specific Runx1-deficient mice developed a spontaneous osteoarthritis (OA)-like phenotype and showed exacerbated articular cartilage destruction under OA, characterized by articular cartilage degradation and cartilage ossification, with decreased Col2α1 expression and increased Mmp13 and Adamts5 expression. The gene discussed is ADAMTS5; the disease is osteoarthritis.