JUN and thrombophilia: On the other hand, multiple signaling pathways may be involved in both diseases such as MAPK (CDC42, HRAS, HSP90AB1, HSPA8, RPS27A, SRC), PI3K-Akt-mTOR (HRAS, HSP90AB1), hypoxia (ACTB, JUN, VEGFA, HIF1A, GAPDH), JAK/STAT (PTPRC, SRC, UBE2I), and NF-kB signaling pathways (ATM, HRAS, IL1B, JUN, PTPRC, SFRS1, TNF) that are the key factors in these patients with hypercoagulation, infection, and inflammation [11, 78].