The β2GPI/anti‐β2GPI complex impairs autophagy, and deficient autophagy plays proinflammatory and prothrombotic roles in APS development.[23, 24] Moreover, SLAMF8/TREM1 exerts crucial functions in restraining the autophagic response.[25, 26] To investigate whether SLAMF8/TREM1 participates in APS pathogenesis by autophagy, cells were subjected to TEM to visualize the formation of autophagic vacuoles. This evidence concerns the gene APOH and autoimmune polyendocrinopathy.