The small GTPase Rac1, also known as Ras-related C3 botulinum toxin substrate 1, is as a positive regulator of chondrocyte hypertrophy and endochondral ossification during bone formation, processes that are recapitulated in osteoarthritis (OA). A new research led by Professor Hong Wei Ouyang shows that inhibition of the aberrant activation of Rac1 in OA, using a novel drug delivery approach, could have therapeutic potential in this disease.