We next inoculated knock-in humanized E16P mEcad (KI E16P) mice, which are permissive to orally-acquired listeriosis, with either EGD ActA+ or ΔC+ strains, to investigate the role of ActA-dependent aggregation in vivo, independent of the critical role of ActA in actin-based motility [4]. This evidence concerns the gene ACTA1 and listeriosis.