Elevated IL-6 and TNF-α levels characteristic of typhoid fever correlate with experimental models showing cytokine-mediated β-cell apoptosis via oxidative stress pathways.[15] These proinflammatory mediators also induce insulin resistance through JNK-1 activation in peripheral tissues, creating a dual metabolic insult that may overwhelm marginal β-cell reserves in predisposed individuals.[16] The mechanism aligns with reports of stress-induced hyperglycemia progressing to irreversible diabetes in sepsis models, though typhoid-specific evidence remains scarce.[17]. This evidence concerns the gene IL6 and typhoid fever.