Our data have shown that HCMV promotes the extended survival of infected monocytes through the prolonged expression of the cellular anti‐apoptotic molecule, Mcl-1 early after infection, which promotes the survival of infected monocytes through a 48-hour viability checkpoint, a time at which uninfected monocytes appear to be programmed to die by apoptosis [25] (Figure 4). This evidence concerns the gene MCL1 and infection.