In particular, significant differential expression was observed in good-responders between pre-treatment and 3 months, attributed to genes in RA-associated pathways that are responsive to relevant upstream regulators including TNF and CSF2 (otherwise known as Granulocyte-macrophage colony-stimulating factor (GM-CSF)), a promising target for therapy in RA [16]. The gene discussed is TNF; the disease is rheumatoid arthritis.