Since MINK1 seems to play a role in osteoarthritis development [200], MINK1 inhibitors could be used to delay OA development and reverse the changes in SMAD2 signaling related to age, but it would be necessary to clarify if MINK1 is responsible for the downfall in SMAD2 phosphorylation or if there are other factors, for example, increased severity of OA in MINK1−/− mice in general, responsible for this effect. Here, MINK1 is linked to osteoarthritis.