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The study of pancreatic ductal adenocarci-noma (PDAC), the fourth leading cause of cancer-related deaths in the U.S., is invari-ably associated with a question: What makes the mortality rate of this tumor almost equal to its incidence rate?1 A median survival time of 20–22 months in patients affected by early PDAC declines to 9–10 months in patients bearing advanced lesions.2 This scenario mainly depends on the clinical and biological features of PDAC, which causes symptoms that vary depending on the location of the tumor within the pancreatic gland and on tumor stage. Although the surgical removal of early PDAC lesions can be curative, such tumors are often asymptomatic or poorly symptomatic and hence often fail to be diagnosed. Conversely, advanced forms of PDAC quickly spread to other organs and are refractory to chemotherapy. From a biological viewpoint, PDAC evolves from a premalignant state to a fully invasive tumor by accumulating genetic and epigenetic mutations that mainly involve the KRAS oncogene and the onco-suppressor genes CDKN2A, TP53 and SMAD4. Although the rapid progression The S100A8/A9 complex reduces CTLA4 expression by immature myeloid cells Implications for pancreatic cancer-driven immunosuppressio