Our published data show that mitochondrial integrity is significantly prolonged by LVS infection, and in keeping with this, BAX mRNA and protein are diminished and BAX translocation to mitochondria is significantly delayed (22, 24), but whether this is attributable to HK2-VDAC interactions at mitochondrial surfaces and/or phosphoinositide 3-kinase signaling remains to be determined. The gene discussed is VDAC1; the disease is infection.