The neutralisation of IL-17A in murine models led to a phenotype with severe colitis.6 At the same time, clinical trials of IL-17 inhibitors reported sporadic cases of autoimmune intestinal inflammation.7 Last, randomised controlled trials (RCTs) of secukinumab in IBD patients led to exacerbation of patients’ symptoms and a higher incidence of fungal infections.8 The above led to the discovery that IL-17A physiologically sustains epithelial barrier function through the regulation of the tight junction protein occludin. Here, IL17A is linked to fungal infectious disease.