Studies have shown that the hypophosphorylated form of UBF blocks rDNA transcription by disrupting the UBF/SL1 complex.151 Others reported that the proliferation rate of cultured neonatal cardiomyocytes is correlated with the phosphorylation of UBF.152 Endothelin-1-induced cardiac hypertrophy is associated with UBF hyperphosphorylation.153 Moreover, enhanced rDNA transcript levels are associated with increased UBF protein levels under α1 adrenergic receptor- or stress-load-induced cardiac hypertrophy. The gene discussed is EDN1; the disease is cardiac hypertrophy.