In reactive MIF, without cell death, a variety of fibrotic signaling pathways in mesenchymal cells (e.g., fibroblasts) may be activated by different stimuli to cause fibrosis, including the following stimuli: mechanical stress associated with pressure overload of HHD and aortic stenosis, defects caused by various causal mutations in sarcomere structure and function of hypertrophic cardiomyopathy, metabolic damage associated with hyperglycemia in diabetic cardiomyopathy, or coronary microvascular endothelial damage in HF with preserved ejection fraction (HFpEF) (Díez et al., 2020). This evidence concerns the gene MIF and hypertrophic cardiomyopathy.