potentially due to redundancy between NFAT family members. To overcome the possible redundancy issue, mice that lack expression of both Nfatc1 and Nfatc2 in chondrocytes (Nfatc1col2Nfatc2–/–mice) were generated. Within a few weeks of birth, the Nfatc1col2Nfatc2–/–mice spontaneously developed severe OA, with many features of human disease, including proteoglycan loss, degradation of collagen and aggrecan, osteophyte formation, flattening of articular surfaces, thickening of the trabecular bone and joint instability.“We intend use this mouse model of OA to determine the mediators of the different catabolic processes. In addition, this model could serve as a platform for us, and others, to test potential new drugs for OA patients,” concludes Greenblatt.