The high physiological significance of this phenomenon is highlighted by a number of myofibrillar myopathies (MFMs) in patients, in which FLNC point mutations potentiate FLNc aggregation, thereby causing an immense formation of larger protein aggregates and impaired protein degradation, which in turn aggravates lesion formation and ultimately leads to the disintegration of myofibrils, muscle weakness, and premature death73–75. This evidence concerns the gene FLNC and myofibrillar myopathy.