Although MVA has the ability to infect DCs which are capable to express and present viral and heterologous antigens to CTLs [68], the abortive viral cell cycle at early stages, the apoptosis induced in DCs after MVA infection (even more accelerated in the case of DCs infected with MVA-C-ΔF1L) and the host cell protein synthesis shutdown, point to the conclusion that cross-presentation could be the dominant pathway for the priming of CD8+ T cells in response to MVA infection [69], [70]. This evidence concerns the gene CD8A and mevalonic aciduria.