On the one hand, type I IFNs boost cross presentation by various mechanisms: first, they stimulate the maturation of DCs; second, they slow the endosome-lysosome acidification process to prevent engulfed tumor antigen clearance and elevate the expression of MHC I molecules on the cell surface [80, 86, 87]; finally, they accelerate DC migration towards lymph nodes, where they can cross-prime tumor-specific CD8+ T cells [88]. The gene discussed is CD8A; the disease is neoplasm.