Dysregulated EGFR function in normal respiratory epithelium and dendritic cells could thus be implicated in the increased risk of severe infection following cetuximab, panitumumab, or zalutumumab therapy, and may also explain excess fulminant infections when EGFR inhibition is added to mTOR inhibition in attempted synthetic lethal cancer therapy, as described in several clinical trials [15]. The gene discussed is EGFR; the disease is infection.