By integrating single-cell transcriptomics and T cell receptor repertoire analyses of regulatory T (Treg) cells in a cohort of patients with acute coronary syndrome from the LILACS trial, Case et al. show that low-dose interleukin-2 clonally expands Treg cells and maintains their suppressive program by bypassing BACH2 downregulation. This evidence concerns the gene BACH2 and acute coronary syndrome.