The recruited cells, mostly of myeloid lineage, secrete IL-6, IL-1α and TNFα to further stimulate STAT3 and NF-κB in a paracrine manner,42,43 and these K-Ras-initiated pathways cooperate to promote the development of PDAC.44 Thus, inflammatory pathways mutually activated in cancer and myeloid cells via tumour-microenvironment crosstalk drive invasion and tumour spread.45,46 We established in vitro that S100A4 and S100A6 are targets of the IL6/IL11-STAT3 pathway, and found that their expression correlates with the presence of pSTAT3 in PDAC samples (Table 1). The gene discussed is KRAS; the disease is neoplasm.