Additionally, MEK-I seems to modulate the immune micro-environment enabling a more permissive immune reaction against the tumor, through different mechanisms: i) inhibition of vascular maturity and integrity and consequent higher immune infiltration in the tumor, ii) direct activation of neutrophils, antigen-presentation cells (APC) such as macrophage and dendritic cells, and of both T-cell subsets, CD8-positive cytotoxic and CD4-positive helper T-cells. The gene discussed is CD4; the disease is neoplasm.