Moreover, spatial resolution studies have shown that B cells are uniformly distributed in the TME but less so near the tumor epithelium; B cells expressing high TGFBI levels, which are similar to regulatory B cells, interact more closely with CD8+ T cells and macrophages [56], suggesting that B cells regulate tumor progression in the PDAC TME through cytokine and chemical stimulation rather than KRAS-related proliferation signals. This evidence concerns the gene TGFBI and neoplasm.