Their research has also suggested that UA can disrupt KRAS-dependent PI3K/AKT/mTOR signaling, reducing stromal fibrosis and enhancing adaptive T-cell responses 52(Figure 8). UA was confirmed to reduce the tumor burden in a preclinical PDAC mouse model by attenuating M2-like tumor-associated macrophages and increasing the number of memory-like CD4+ and CD8+ T cells. This evidence concerns the gene AKT1 and neoplasm.