There are a number of other conditions, sometimes referred to as autoinflammatory syndromes because of the lack of high-titer autoantibodies or antigen-specific T-cells that are also characterized by episodic inflammation. Seven are caused by mutations in five other genes: the TNF-receptor associated periodic syndrome (TRAPS) is caused by mutations in one of the receptors for tumor necrosis factor (TNF); the hyperimmunoglobulinemia D with periodic fever syndrome (HIDS) is caused by mutations in the gene encoding mevalonate kinase; Muckle-Wells syndrome (MWS), familial cold autoinflammatory syndrome (FCAS), and neonatal-onset multisystem inflammatory disease (NOMID) are caused by mutations in the gene encoding cryopyrin, a member of the aforementioned pyrin family of proteins; deficiency of the interleukin-1 receptor antagonist (DIRA) is caused by mutations in the gene that codes for the interleukin-1 receptor antagonist, a protein that helps to regulate levels of the inflammatory cytokine, interleukin-1; and the syndrome of pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) is caused by mutations in PSTPIP1, a protein that binds pyrin. In addition, there are patients with episodic fevers and/or inflammation who do not have identifiable mutations in any of these genes. Some of these latter cases appear to cluster in families, while others are sporadic.