While the particular binding of CTLA-4 to B7 (mainly CD80 or CD86) is enhanced, that leads to competitive inhibition of CD28/B7 co-stimulatory signals, thus inhibiting T-cell growth and triggering, resulting in decreased secretion for cytokines such as IL-2, IL-4, IFN-γ, as well as decreased expression for IL-2 receptor, which creates the condition for tumor cells to escape immune surveillance and makes the rapid development of tumors [14, 15]. This evidence concerns the gene CD86 and neoplasm.