The authors reported that tumor-derived IL-1, released by tumor cells and inflammasome adaptor ASC-activated M2 cells, is crucial for TSLP secretion by CAFs (22) (Figure 1A), and that IL-4 derived by basophils, recruited into TDLNs by alternatively activated M2 macrophages, stabilizes the Th2 polarization (56) (Figure 1C), thus adding further complexity to the crosstalk within the tumor microenvironment that leads to predominant Th2 inflammation in pancreatic cancer (57). The gene discussed is TSLP; the disease is neoplasm.