Activated PSCs enable cancer cells to resist gemcitabine via the Notch pathway-mediated Hes1 overexpression[188], exclusive expression of periostin in PSCs[189], and the paracrine stromal cell-derived factor (SDF)-1α-mediated activation of FAK/Akt and extracellular signal-regulated kinase (ERK)1/2, with subsequent activation of the IL-6/Janus kinase (JAK)/STAT3 pathway in the tumor cells in an autocrine manner[190]. The gene discussed is STAT3; the disease is neoplasm.