Limiting TNF-based pro-inflammatory responses also improves symptoms in patients homozygous for rare variants in OTULIN and suffering from an autoinflammatory syndrome called OTULIN-related autoinflammatory syndrome (Damgaard et al., 2016) or otulipenia (Zhou et al., 2016). The gene discussed is OTULIN; the disease is autoinflammation, panniculitis, and dermatosis syndrome, autosomal recessive.