These factors have been linked to pro‐tumor effects, including cancer cell survival, proliferation, myeloid recruitment, angiogenesis, and immune evasion [53, 54, 55, 56], and many are regulated downstream of redox‐sensitive transcriptional pathways linked to PDI and ER stress (e.g., via the PERK/NF‐κB and IRE1/TRAF2 axes) [57, 58, 59]. The gene discussed is NFKB1; the disease is neoplasm.