In agreement with other studies, we found that lung Trm cells were perfectly able to expand locally in response to infection without the need to recruit peripheral M2e-specific effector or central memory CD4 T cells, as assessed in our FTY720-treatment experiments.10,53 In the Tbx21-deficient mouse model anti-IL-17 mAb treatment failed to reduce the level of protection, hence, arguing for an important role of IFNγ.51 However, we did not find significant Tbx21 or Ifnγ gene expression in expanded M2e-specific Th17 Trm cells upon infection, (scRNAseq data). The gene discussed is CD4; the disease is infection.