Indeed, knock-out experiments have shown that human cell lines lacking GBP1 fail to resolve intracellular pathogen infections while epidemiological evidence in humans heavily implicates polymorphisms in GBP1 with chronic active Epstein-Barr virus infection, ulceroglandular tularemia, and elevated GBP1 in the cerebrospinal fluid of patients with bacterial meningitis (33, 50). This evidence concerns the gene GBP1 and tularemia.