To determine whether the formation of TIFs in LT-HSCs was due to ATR signaling, we then measured the expression of replication protein A 32 kDa subunit (RPA32, a ssDNA binding protein that activates the ATR kinase pathway8) and phosphorylated Chk1 (pChk1, which has a critical role in DNA damage checkpoint control and tumor suppression26, 27) by immunocytochemistry, following BMT of control GFP or Pot1a overexpressing HSCs. The gene discussed is ATR; the disease is neoplasm.