OA, which is one of the most common joint diseases, is a leading cause of disability and is becoming a worldwide burden with economic costs.22 Despite its increasing significance, no approved therapies can prevent the progression of OA, and no consensus has been reached on the pathological mechanism of OA due to its multiple etiologies.23 In the current study, we examined the important role of Runx1 in OA and its potential therapeutic effect in a mouse model from a genetics perspective. This evidence concerns the gene RUNX1 and arthropathy.