After eCPMV inhalation, tumor‐infiltrating neutrophils and activated neutrophils significantly increased, leading to a delayed growth of tumor and rejection to a secondary challenge.[133] The immunogenicity of eCPMV was proved to be controlled by MyD88‐dependent TLR2 and TLR4 signaling.[138] This neutrophil‐based antitumor strategy was successfully applied in multiple tumor models, including lung, skin, ovarian, colon, and breast cancers.[133]. The gene discussed is TLR4; the disease is neoplasm.