Notably, although LEC1 ECs were exceptionally rare (<1.5%) in hearts from all groups and time points, they were most abundant in CTL hearts on P1 and in MIP28 and ARP1MIP28 hearts on P30 (Figure 1I; Supplementary Figure S4), and were enriched for many of the same mitosis/cytokinesis markers, gene ontology terms, and transcription factors that were upregulated in VEC1 ECs (Figure 2G), which suggests that expansion of the LEC1 cluster may have a role in the inflammatory response (Prabhu and Frangogiannis, 2016) and/or contribute to the re-uptake of interstitial fluid after MI. The gene discussed is ADGRL2; the disease is myocardial infarction.