Primary abnormalities of LV active relaxation, increased passive LV stiffness (because of myocardial fibrosis, glycation of collagen, titin isoform shift and impaired titin phosphorylation), and impaired atrial mechanical function, may each contribute to impaired diastolic filling at rest in HFpEF.5, 33 This results in raised LVEDP and an impaired ability to use the Frank‐Starling mechanism to increase stroke volume. The gene discussed is TTN; the disease is Myocardial fibrosis.