Murine embryonic fibroblasts exposed to 1 μM gliotoxin in vitro undergo apoptosis in a Bcl-2 homologous antagonist/killer (Bak) dependent manner (Pardo et al., 2006), while immunosuppressed Bak–/– mice that received an intranasal inoculation of gliotoxin-producing A. fumigatus were more resistant to infection compared with wild-type controls, highlighting the role of Bak as critical factor involved in gliotoxin-mediated cell death (Pardo et al., 2006). Here, BAK1 is linked to infection.