As a key regulator in mounting immune responses against fungal infection, SYK activation is tightly regulated by phosphorylation of the dual tyrosine residues in the linker and kinase domains.16 In resting state, the two N-terminal SH2 domains of SYK are distorted in a way preventing its binding with the ITAM motif of Dectin-1/FcRγ, thus SYK is kept in an inactive state. This evidence concerns the gene FCER1G and fungal infectious disease.