Like many patients with cancer, mice with LLC tumors are poorly responsive to blockade of PD-1/PD-L1 signaling.2–5 Direct CDA treatment induced rapid and significant increase in PD-L1 gene transcription in tumor lesions (figure 2A) and TDLNs (figure 2B), and elevated PD-L1 expression was sustained for at least 6 hours in both TME sites. This evidence concerns the gene PDCD1 and neoplasm.