Inhibition of LTB4 synthesis in patients with COVID-19 was unable to reduce the duration of symptoms.135 Moreover, previous work suggested that LTB4 could enhance Type I IFN levels and pulmonary neutrophil responses in influenza-infected mice, correlating with improved outcomes of infection.136–137 However, while mice lacking BLT1 have increased mortality after influenza infection, this was traced to increased immune pathology rather than altered viral control.138. The gene discussed is LTB4R; the disease is infection.