TNFRSF12A is the smallest member of the Tumor Necrosis Factor Receptor superfamily[8] and the gene expression is highly regulated in a live organism and a petri dish.

[13] For further context, the CRD's tertiary structure consists of a beta-sheet with two strands, followed by a 3(10) helix and a C-terminal alpha-helix, and is held together by three disulfide bonds that connect Cys36-Cys49, Cys52-Cys67, and Cys55-Cys64.

[6] Gene expression was also found in many of the major organs of newborn animals, and in the adult heart, kidney, lung, ovary, and skin.

[9] What makes TNFRSF12A stand out other than its size from the other Tumor necrosis factors receptor superfamily is that the gene expression is extremely regulated in a live organism and in a petri dish.

[11][8] Increased expressions or interactions of TNFRSF12A and TNFRSF12 have been found to correlate with diseases and morbidity such as acute ischemic stroke, Rheumatoid Arthritis, Systemic Lymphocytic Erythematosus (SLE), Multiple Sclerosis and Cancer.

[9][16][8][11] In a clinical study, the overall severity of the disease was found to be reduced by intraperitoneal injection of an anti-TWEAK neutralizing monoclonal antibody in rats and mice.

[8] The result of the clinical study implied that Fn14 was a tumor biomarker and that it should be taken into account as a potential new cancer treatment target.