To protect the body from infection, immune cells in the lungs can exploit cell death programs in inhaled fungal pathogens, scientists have revealed, helping explain why most people aren't harmed by breathing in mold spores, and potentially offering new therapeutic strategies for people who do get infected. Humans inhale anywhere from 1,000 to 1010 mold spores daily. In order to prevent harmful fungal infection, neutrophils and other immune cells that "devour" cellular bodies help clear inhaled spores from the lungs. However, individuals with immune systems already weakened by tuberculosis, autoimmune disease, AIDS or chemotherapy, to name a few, can more easily contract disease from exposure to mold. To develop effective therapies for these individuals, a clearer picture of anti-fungal immunity is needed. In mice, Neta Shlezinger and colleagues studied how immune cells in the lungs combat Aspergillus fumigatus, the most common mold-related pneumonia worldwide. They discovered that lung neutrophils engulfed the spores and then triggered the fungi's own "programmed cell death" pathway, preventing fungal germination and host invasion. Importantly, the authors also found an A. fumigatus protein called AfBIR1, the fungal equivalent of the human Survivin protein known to suppress cell death and prolong tumor growth, resisted cell death. Mice exposed to spores overexpressing AfBIR1 readily developed fatal fungal infections. Pharmacologic inhibition of BIR1 encoding for AfBIR1 increased fungal cell death and clearance in infected airways, suggesting that blockade of AfBIR1 could be a viable therapeutic approach against invasive aspergillosis.