Additionally, the failure of murine studies in unequivocally showing the role of Dectin-1 and Th17 response during systemic and mucosal Candida infection reveals (1) the possible involvement of different CLRs, (e.g., Dectin-2, Dectin-3); (2) how the confounding results obtained by using different models could rely on the site-specific requirements of peculiar cells to properly cope with the diverse Candida morphotypes; (3) how immune outcomes can be influenced by the strains used as infection agent. This evidence concerns the gene LARS1 and candidiasis.