We speculated that loss of Setd2 reprogrammed neutrophils to form an immunosuppressive TME, thereby allowing tumor cells to evade immune surveillance.[13] Given that the proportion of CD8+ T cells did not differ significantly upon Setd2 loss (Figure 1C–F), we speculated that the cytotoxicity of CD8+ T cells might be altered in Setd2‐deficient pancreatic tumors. This evidence concerns the gene CD8A and neoplasm.