For example, the patients with ITP displayed abnormalities in BM-MSCs, due to defects in mRNA and miRNA that induced downregulation of genes involved in cellular stress machinery, such as the unfolded protein response (UPR), the nuclear protein transcriptional regulator 1 (Nupr1), involved in endoplasmic reticulum pathway, the TGF-β1 signaling, leading to a loss of immunosuppressive properties, and a breakdown of self-tolerance in ITP patients [222]. Here, DR1 is linked to autoimmune thrombocytopenic purpura.