A series of preclinical experiments supported a model whereby FAK activity in PDAC cancer cells led to cytokine production that promoted a fibrotic and immunosuppressive TME rich in CAFs, myeloid-derived suppressor cells, and regulatory T cells (Tregs); small-molecule inhibition of FAK reversed these phenomena and led to an increase in CD8+ T cells that controlled tumor growth, as well as a potentiated response to immune checkpoint inhibition. Here, CD8A is linked to neoplasm.