Although rapamycin post-transcriptionally downregulated KLF2 expression, infection with Klf2-expressing AAV was sufficient to restore its expression in murine EC and subsequently rescue EC-dependent vasodilation in RptorEC−/− mice, strengthening the causal relationship between decreases in KLF2-induced eNOS and impairment of EDD in the mTORC1-inhibited artery. This evidence concerns the gene KLF2 and infection.