While the complete genetic deletion of pro-inflammatory cytokines, particularly TNF-α, IL-1α/β, or IFN-γ, increases disease susceptibility in invasive fungal infections (Lionakis and Netea, 2013; Cheng et al., 2012; Gow et al., 2012; Netea et al., 2008, 2010), excessive inflammation causes collateral damage to the host (Carvalho et al., 2012; Romani et al., 2008), indicating that efficient protection against fungi requires a fine-tuned balance between pro-inflammatory effector and counter-regulatory immune mechanisms. Here, IL1A is linked to fungal infectious disease.