ΔNp63 and Stat3 are involved in several common pathways regulating CSC properties (1, 7), Stat3 is a direct regulator of ΔNp63 transcription (9, 10) and they cooperate in regulating epithelial cell identity in KRas-driven lung and pancreatic cancers (25), whilst ΔNp63 overexpression itself alters pTyr705- and Ser727-Stat3 levels in TNBC cells (55). This evidence concerns the gene STAT3 and pancreatic neoplasm.