It provides evidence linking Cpt1a deficiency to infection susceptibility and impaired neutrophilic responses in both humans and mouse models, demonstrates impaired neutrophil mobilization in response to infection and G-CSF-induced mobilization, and establishes the requirement of Cpt1a-dependent FAO for neutrophil chemotaxis using genetic knockdown, multiple pharmacologic inhibitors, substrate depletion, and rescue with the addition of the Cpt1a-independent fatty acids, octanoic acid, acetate, and propionate. Here, CSF3 is linked to infection.