Neutrophils in the joints of RA patients activate RIPK1, RIPK3, and MLKL under the influence of CD44 and granulocyte-macrophage colony-stimulating factor (GM-CSF) to cause necroptosis, which can be blocked through the application of fibroblast activation protein-α (FAP-α) suggesting its importance as an potent drug for RA treatment (171). The gene discussed is RIPK3; the disease is rheumatoid arthritis.