CRYAB and heart failure: These observations support a novel paradigm that dysregulation of biomolecular condensates, as observed in rare genetic cardiomyopathies triggered by the R636S mutation in RBM20 (a striated muscle-specific nuclear alternative splicing factor (43)) and with the R120G mutation in CRYAB (vide supra), may be pathogenic in common etiologies of cardiomyopathy, opening the door for targeting biomolecular condensates to develop sarcomere-targeted therapies for highly prevalent causes of heart failure.