“…Previous studies had shown that pathways include neutrophil degranulation [74], immune system [75], extracellular matrix organization [76], toll-like receptor cascades [77], cytokine signaling in immune system [78], metabolism of RNA [79] and gene expression [80] were involved in the progression of CF. NTRK3 [81], MMP9 [82], IGF2 [83], SOCS3 [84], IGFBP2 [85], SLC1A3 [86], NOS1AP [87], HP (haptoglobin) [88], TLR5 [89], ARG1 [90], NRG1 [91], RGS5 [92], LCN2 [93], TSPO (translocator protein) [94], PLAU (plasminogen activator, urokinase) [95], MME (membrane metalloendopeptidase) [96], BST1 [97], NR6A1 [98], TLR4 [99], NRN1 [100], ABCA13 [101], CTSD (cathepsin D) [102], NCAM1 [103], SIGMAR1 [104], CNR2 [105], CCR4 [106], ABCB1 [107], TIMELESS (timeless circadian regulator) [108], IRF8 [109], TXNIP (thioredoxin interacting protein) [110], SUV39H1 [111], CRY1 [112], CRY2 [113], PDCD4 [114] and MGAT5 [115] played an important role in depression and anxiety. Accumulating evidence has demonstrated that MMP9 [116], S100A12 [117], HP (haptoglobin) [118], TLR5 [119], NRG1 [120], PLAU (plasminogen activator, urokinase) [121], SLC11A1 [122], AQP9 [123], CHIT1 [124], TLR4 [125], SLC26A8 [126], CTSD (cathepsin D) [127], SERPINB1 [128], FASLG (Fas ligand) [129], SLC4A4 [130], AQP3 [131] and IRF8 [132] appears to be constitutively associated with CF .…”