To better understand the infection pattern in different cell types when BAX/BAK were not suppressed, we evaluated the replication of double-deficient viruses in cultured primary macrophages, and immortalized fibroblasts as well as endothelial cells, all of which support parental K181 replication but show differential susceptibility to various MCMV mutants [30] consistent with cell type-specific function of virus-encoded cell death suppressors (Figure 1D–F and Figure S1B–E). The gene discussed is BAX; the disease is infection.