This analysis revealed integrins (e.g., ITGB3, ITGA2B), focal adhesions and cytoskeletal rearrangements (e.g., PTK2, MYLK, MYL9), SRC/RAS signaling components (e.g., SRC, RASD1, RASGRP1), chemokines (e.g., CXCL1, CCR4, CXCL3), and PI3K/AKT/MTOR signaling (e.g., AKT3) as being some of the key dysregulated molecules in third-tercile APS patients (Supplementary Fig. 16). This evidence concerns the gene CXCL3 and autoimmune polyendocrinopathy.