In the hypervirulent KPPR1 strain, yersiniabactin was specifically shown to contribute to bacterial replication in murine respiratory tracts, in part by evading the host innate immune protein lipocalin 2 (LCN2) [70–72] However, in a recent study of convergent strains, the presence of yersiniabactin and aerobactin-encoding genes in HMV-negative strains did not appreciably affect virulence in a murine pneumonia model [49]. This evidence concerns the gene LCN2 and pneumonia.