Interestingly, CIN- and STING-dependent ligands that measurably impacted recipient cells in the TME were associated with an unfolded protein response (UPR) to endoplasmic reticulum (ER) stress, in addition to canonical pathways associated with CIN such as NF-κB and IL6-Jak-Stat3 signalling2,31, whereas effectual ligands emanating from CINlow or Sting1-depleted CINhigh tumour cells were associated with IFN responses (Fig. 4b–d). The gene discussed is NFKB1; the disease is neoplasm.