Our results showed upregulated apoptosis level in CS-inhibited cancer cells might contribute to the reduced cell proliferation capacity and the increased drug sensitivity. Through PF-4217903 microarray analysis and real-time PCR, we discovered that knockdown of CS led to IRF7, ISG15, DDX58, and CASP7 expression being increased in SKOV3 and A2780 cells, whereas ATG12 expression was decreased. CASP7 encodes Caspase 7 and is involved in the caspase activation cascade responsible for the execution of apoptosis. IRF7 encodes one of the interferon regulatory factors and is required in breast cancer cells to prevent immune escape-mediated bone metastasis. Elevated expression of IFN-stimulated gene 15, which encodes a protein that antagonizes the ubiquitin/proteasome pathway, has been shown to confer camptothecin sensitivity in breast cancer cells in part by interfering with topoisomerase I downregulation. DEAD box polypetide 58 encodes a cytoplasmic pathogen recognition receptor that recognizes pathogen-associated molecular pattern motifs that differentiate between viral and cellular RNAs. The RIG-I pathway is tightly regulated and aberrant signaling leads to apoptosis, altered cell differentiation, inflammation, autoimmune diseases, and cancer. Notably, IRF7, ISG15, and DDX58 contribute to chemosensitivity in breast cancer and CASP7 encodes a proapoptotic protein that may make cancer cells more sensitive to chemotherapy. Finally, ATG12 is the human homolog of a yeast protein necessary to form autophagic vesicles. Given that treatment with DDP has been shown to enhance reactive autophagy, the downregulation of ATG12 observed upon CS silencing in SKOV3 and A2780 cell lines is consistent with our observations of decreased drug resistance. The diagram was shown to clearly identify potential signaling pathways modulated by CS. Taken together, these findings demonstrated that abnormally upregulated expression of CS was found in human ovarian carcinoma, modulating its expression can influence cell proliferation, invasion, migration, and chemosensitivity of SKOV3 and A2780 cells. We thus propose that CS inhibition represents a novel therapeutic intervention to improve the prognosis of patients with ovarian cancer by suppressing metastasis and overcoming resistance of chemotherapy. As CS takes part in a complicated network in the organism metabolism, how CS is regulated in human ovarian carcinoma needs to be further explored. Graft-versus-host disease, a representative of T cell-mediated immune responses, remains a significant cause of morbidity and mortality in patients undergoing bone marrow transplantation. Billingham’s tenets reflect the three basic principles in the development of GvHD. Additionally, some investigations highlighted that the effector cells migrating to the target tissues is important for the development of GvHD. FTY720 inhibited GvHD lethality by preventing lymphocyte egress from Secondary lymphoid organs to peripheral organs. Corticosteroids, the first-line therapy of GvHD, make lymphocytes trafficking into bone marrow, but away from lymph nodes and inflammatory.