While inborn errors of the type I interferon (IFN) pathway have been primarily associated with severe viral infections,22 and genetic deficiencies in the IL-17 pathway are classically linked to chronic mucocutaneous candidiasis and other opportunistic infections, emerging evidence indicates that patients with these defects may also exhibit an increased susceptibility to bacterial infections, including those caused by encapsulated pathogens such as S. pneumoniae.23 This evidence concerns the gene IFNA1 and chronic mucocutaneous candidiasis.