Therefore, it seems clear that if in vivo exposures to HDPs within a localized infection (as in the current animal model) are playing a role in the emergence of DAP-R, it likely requires exposure of the infecting strain to either: i) multiple HDPs from neutrophils and/or platelets; ii) combinations of HDPs; iii) higher peptide concentrations reflecting those likely to exist in vivo; and/or iv) additional host factors. This evidence concerns the gene PLEKHM3 and infection.