Investigations into PDAC have elucidated that this process can be explained by the synergistic interactions involving TGF-β signaling, the expression of the B cell chemoattractant CXCL13 by tumor-reactive T cells, and the supportive role of fibroblast-derived TGF-β, which collectively enhance the activation of B cells [179]. The gene discussed is TGFB1; the disease is neoplasm.