FGF16 and cardiac hypertrophy: After injury, the mutant hearts also display impaired coronary angiogenesis and increased hypertrophy and fibrosis with a significant reduction in the expression of FGF16. The cardiac-specific overexpression of FGF16 in the mutant hearts partially rescues cardiac hypertrophy, promotes cardiomyocyte replication, and improves heart function after injury, indicating that GATA4 is required for neonatal heart regeneration through the regulation of FGF16, which has potential in promoting myocardial repair (Yu et al., 2016).