β-arrestin1 mRNA levels and nuclear accumulation of β-arrestin1 protein were significantly increased in the CD34+ cells of patients with low-risk disease compared to higher-risk MDS or healthy controls, and inhibition of β-arrestin1 in cultured CD34+ cells mitigated TLR2 agonist-induced cell death (70). This evidence concerns the gene TLR2 and myelodysplastic syndrome.