TGFB1 and heart failure: Integrated analysis of global chromatin accessibility landscapes and single‐cell transcriptomic profiling demonstrated compromised TGF‐β signaling within hematopoietic stem cells, which facilitated the establishment of a “stress memory” phenotype.[249] This epigenetic reprogramming amplified the capacity of hematopoietic stem cells to generate pro‐inflammatory macrophages.[249] This study suggests that increasing the level of TGF‐β may be a novel strategy for the treatment of recurrent heart failure and related complications.