Although CDA-2 was suggested to contribute to tumor inhibition through the up-regulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) and repression of PI3/Akt signaling pathway in tumor cells, the tumor-inhibiting effect of CDA-2 was so far mainly demonstrated in cancer cells and its action in tumor microenvironments, especially to immune/inflammatory cells in tumor stroma, has not been critically evaluated [6], [7]. The gene discussed is AKT1; the disease is neoplasm.