Given that gemcitabine also induces replication stress and activates ATR/Chk1 to trigger DNA damage response, the combined activation of ATR/Chk1 signaling by A3 protein expression and gemcitabine treatment may synergistically enhance cellular tolerance to replication stress, thereby promoting tumor cell survival and resistance to gemcitabine. The gene discussed is CHEK1; the disease is neoplasm.