A recent study demonstrated that the gain‐of‐function Trp53R172H mutation promoted the accumulation of neutrophils in pancreatic tumors.[18] We observed that loss of Setd2 could enhance neutrophil accumulation in pancreatic tumorigenesis, from KrasG12D‐induced precancerous pancreatic intraepithelial neoplasia (PanIN) to malignant pancreatic tumors with KrasG12D/+ and Trp53R172H/+ mutations. Here, SETD2 is linked to pancreatic neoplasm.