Histoplasmosis is reported in patients with HIES resulting from loss-of-function mutations in STAT3 (Robinson et al., 2011; Odio et al., 2015), as well as gain-of-function mutations in STAT1 (Sampaio et al., 2013); this could be related to impaired Th17 responses, other perterbations resulting from loss of these transcription factors, or a combination of Th17-dependent and Th17-independent factors. Here, STAT3 is linked to hyper-IgE syndrome.