“…12 Moreover, OVs can activate various forms of immunogenic cell death (ICD), including immunogenic apoptosis, necroptosis and pyroptosis, by inducing endoplasmic reticulum (ER) stress, 77,78 leading to the release of hallmark immunostimulatory damage-associated molecular patterns (DAMPs), such as ATP, high mobility group box 1 protein (HMGB1), heat shock protein, ectocalreticulin and proinflammatory cytokines. 79,80 These PAMPs and DAMPs are sensed by pattern recognition receptors (PRRs), such as stimulator of IFN genes (STING), Toll-like receptor (TLR) adaptor molecule 1 and TLR3 on immune cells, [81][82][83] establishing a proinflammatory microenvironment by stimulating the production of proinflammatory cytokines, such as type I IFNs, interleukin (IL)-1β, IL-6, IL-12, TNF-α, GM-CSF, and chemokines, such as CCL2, CCL3, CCL5, and CXCL10, leading to the transformation of immunologically "cold" tumors into "hot" tumors. 71 First, locally secreted chemokines, such as CCL3 and CXCL10, recruit the first cell responders, such as neutrophils and macrophages, to the site of infection, 84 and these cytokines are involved in the induction of effective antitumor responses.…”