Several factors are likely to have a role in PaCS origin: (1) cell differentiation and activation by cytokines and trophic factors, as in cultured DCs, NK cells and ANKRD26-mutated megakariocytes; (2) cell activation and transformation by oncogenic microbial products, as in H. pylori gastritis [78] and HPV oncogene-expressing HeLa cells [39]; (3) leukemia-prone mutations, as in Shwachman–Diamond neutropenia [79] and ANKRD26-related thrombocytopenia [80], [81]; or (4) apparently non-mutated, constitutive overexpression of EGF receptor, as for pancreatic serous cystic adenoma [46]. This evidence concerns the gene ANKRD26 and leukemia.