Studies have shown that CAFs in direct contact with tumor cells activate TGFβ signaling and collagen deposition, while CAFs farther away from the tumor promote hyaluronic acid deposition and reshape the TME by secreting IL-6 and other inflammatory mediators.9 Moreover, emerging evidence suggests that CAFs promote chemoresistance primarily by disrupting drug delivery and biochemical signaling within tumor cells. The gene discussed is TGFB1; the disease is neoplasm.