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A study has shown that lixisenatide inhibits inflammation of RA in human FLSs by downregulating IL-6, IL-8 and TNF-, while also inhibiting cellular communication pathways including c-Jun N-terminal kinase (JNK) and NF-B [239]

thus, the phenotype is manifest fully in males whereas female heterozygotes display varying degrees of G6PD deficiency, due to alternate X-chromosome inactivation 3,4