Notably, it is currently known that the neutrophil extracellular traps (NETs) could induce naïve CD4+ T cell differentiating into a Th17 phenotype,[40] and the NETosis is recognized as an important event involved in the pathogenesis of SLE and APS, especially in thrombotic APS.[41] Further mechanistic studies are warranted to elucidate the complex interplay between NETosis and Th17 cells contributing to the thrombotic APS. Here, CD4 is linked to autoimmune polyendocrinopathy.