VV F1L has been shown to inhibit the mitochondrial pathway of apoptosis by replacing Mcl-126 and interacts with the isolated BH3 domains of Bim, Bax and Bak,23 which are bound in the canonical Bcl-2-binding groove.22 Furthermore, an F1L-deficient VV potently causes Bak/Bax-mediated apoptosis.15, 27 Functionally, VV F1L appears to rely primarily on neutralization of Bim in the context of a viral infection.22 Given the close similarity between VAR and VV, VAR may also rely on inhibition of host cell apoptosis for successful infection and proliferation. The gene discussed is BAK1; the disease is infection.