If one copy of the CREBBP gene is deleted or mutated, cells make only half of the normal amount of CREB binding protein. A reduction in the amount of this protein disrupts normal development before and after birth, leading to the signs and symptoms of Rubinstein–Taybi syndrome.Mutations in the EP300 gene are responsible for a small percentage of cases of Rubinstein–Taybi syndrome. These mutations result in the loss of one copy of the gene in each cell, which reduces the amount of p300 protein by half. Some mutations lead to the production of a very short, nonfunctional version of the p300 protein, while others prevent one copy of the gene from making any protein at all. Although researchers do not know how a reduction in the amount of p300 protein leads to the specific features of Rubinstein–Taybi syndrome, it is clear that the loss of one copy of the EP300 gene disrupts normal development.A mouse model has been identified in order to perform experimental research procedures. The model has exhibited the same clinical symptoms seen in humans and has become a foundation for future research.Unfortunately, in nearly 40% of cases, neither gene, CREBBP or EP300, can be implicated in the cause of the disease. In these cases, there is no mutation on the 16th chromosome leaving many more questions yet to be answered.
Indications for beta blockers include:

Angina pectoris (contraindicated for Prinzmetals angina)
Atrial fibrillation
Cardiac arrhythmia
Congestive heart failure
Essential tremor
Glaucoma (as eye drops, they decrease intraocular pressure by lowering aqueous humor secretion)
Hypertension, although they are generally not preferred as an initial treatment
Hyperthyroidism
Migraine prophylaxis
Mitral valve prolapse
Myocardial infarction
Phaeochromocytoma, in conjunction with α-blocker
Postural orthostatic tachycardia syndrome
Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism
Theophylline overdoseBeta blockers have also been used for:
Acute aortic dissection
Hypertrophic obstructive cardiomyopathy
Long QT syndrome
Marfan syndrome (treatment with propranolol slows progression of aortic dilation and its complications)
Prevention of variceal bleeding in portal hypertension
Possible mitigation of hyperhidrosis
Social and other anxiety disorders
Controversially, for reduction of perioperative mortality in non-cardiac surgery, but the best evidence suggests that they increase mortality when used this way

Congestive heart failure
Although beta blockers were once contraindicated in congestive heart failure, as they have the potential to worsen the condition due to their effect of decreasing cardiac contractility, studies in the late 1990s showed their efficacy at reducing morbidity and mortality.Bisoprolol, carvedilol, and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in congestive heart failure, although at doses typically much lower than those indicated for other conditions. Beta blockers are only indicated in cases of compensated, stable congestive heart failure; in cases of acute decompensated heart failure, beta blockers will cause a further decrease in ejection fraction, worsening the patients current symptoms. Beta blockers are known primarily for their reductive effect on heart rate, although this is not the only mechanism of action of importance in congestive heart failure.