Tumor necrosis factor‐alpha (TNF‐α) is a 233 amino acid, 17 kilodalton, homotrimer, bell‐shaped proinflammatory cytokine. TNF‐α is usually secreted from monocytes and macrophages and is also an inducer of many proinflammatory cytokines like IL‐1, IL‐6 and others to help regulate immune cell function. . TNF‐α has two transmembrane cell receptors, TNF‐R1 and TNF‐R2, which have functional binding domains located on the outside of the cell and catalytic signaling domains located inside the cell. TNF‐R1 mediates the activation of a number of transcription factors resulting in an increased inflammatory response, while TNF‐R2 increases the number of T‐cells through a proliferation/survival pathway. A high amount of TNF‐α compared to a low number of its receptors leads to joint inflammation and eventual shock, while a low amount of TNF‐α leads to cachexia. Rheumatoid Arthritis (RA) has many causes including environmental factors, proclivity of smoking, or a genetic history, but in all cases, TNF‐α seems to play a role in disease progression due to its high proteins concentration in advanced disease stages. The source of TNF‐α in joints could be due to the production of the protein by CD4+ T cells in the synovial fluid which has been associated with synoviocyte proliferation, osteoclast activation, and cartilage degradation. Attempts to inhibit TNF‐α are currently centered around general suppression of the protein through TNF‐α inhibitors, but due to the devastating effects these treatments have on the immune system, further studies are considering creating higher numbers of anti‐inflammatory cytokines to create a balance between inflammatory and anti‐inflammatory cytokines, while other studies are attempting to target downstream protein targets of TNF‐α in an attempt to selectively suppress disease symptoms. The Walton High School SMART Team has designed a 3D model of TNF‐α using JMOL to investigate the relationship between structure and function.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.