It was also observed that the presence of AD-MSCs triggered a decrease in NPCy apoptosis via the blockade of caspase-3 and 9 as well as augmentation of ECM genes with decreased secretion of metalloproteinases and proinflammatory cytokines like IL-1β, IL-6, and TNFα in a coculture experiment involving AD-MSCs and NPCy at a prolonged compressive loading of 3 MPa for 48 h (Figure 2) [4, 88]. The gene discussed is IL1B; the disease is Alzheimer disease.