Figure 4B shows that the CD11b+Ly6G+FAS+ population, which induces tumor-cell apoptosis, is an N1 neutrophil population [24] that was significantly increased in melanoma tissues treated with the combination therapy (6.1±3.1%) compared with HVJ-E (2±0.3%) or poly I:C (2±0.9%) treated therapies, whereas the expression levels of VEGF and MMP9, which are proangiogenic markers for N2 neutrophils [24], were decreased in CD11b+Ly6G+ neutrophils in response to the combination treatment compared with control (Supplementary Figure S3). The gene discussed is VEGFA; the disease is neoplasm.