A step forward into our understanding of the functional relevance of the neutrophilic NLRP3 inflammasome arose from Pearlman’s lab [92,93], who elegantly demonstrated using gene-targeted mice and in vivo depletion that neutrophils represented a prime source of IL-1β in a NLRP3-, ASC- and caspase-1/11-dependent manner during Streptococcus pneumoniae (serotype 4) corneal infection. This evidence concerns the gene IL1B and corneal infection.