Although MK2 inhibitors may not be as useful therapeutically as p38 inhibitors, if the accelerated cell aging seen in WS does underlie the accelerated whole body aging, they may prove useful in the alleviation of the associated inflammatory conditions that are thought to be MK2 dependent and have certainly helped to suggest a role for p38-activated MK2 in replicative senescence in WS fibroblasts. Here, MAPKAPK2 is linked to Werner syndrome.