The principal findings were as follows: (1) in diabetes patients with HFrEF, a reduction in thoracic SMI was more likely to be associated with a deterioration in LV contractility, together with an increase in LVM and a heavier burden of myocardial fibrosis, leading to “nonfunctional” cardiac hypertrophy; (2) thoracic SMI, rather than BMI, was independently associated with the level of NT-proBNP; and (3) a lower thoracic SMI indicated a higher risk of adverse clinical outcomes, regardless of cardiac functional/structural measurements. The gene discussed is NPPB; the disease is Myocardial fibrosis.