Cancer-derived exosome HSPC111 is capable of not only inducing the transformation of fibroblasts into CAFs within the PMN, but also phosphorylating ACLY to elevate acetyl-CoA levels and influence the lipid metabolism of these CAFs.125 This not only enhances the immunosuppressive milieu of the PMN but also facilitates the proliferation and metastasis of cancer cells through heightened expression and activity of ACLY.211–213 Despite the scarcity of research on metabolic reprogramming within the PMN, the significance of metabolism in cancer metastasis is undeniable. This evidence concerns the gene NOP16 and cancer.