FHS is also in the differential, which logically agrees with the thought that the disease is a result of a mutation in SRCAP, as this gene interacts with CBP. Behavior
Tantrums during infancy
Attention deficit-hyperactivity disorder (ADHD) during school years: impulsivity, inattention, restlessness
Unpredictable, aggressive outbursts
Autistic spectrum disorder (one case)
Asperger syndrome (one case)
Obsessive compulsive disorder (two cases)

Other observations
Intellectual disability: in all cases each individual showed a varying degree of intellectual impairment and learning disability, ranging from borderline normal to moderate intellectual disability
Early entry into puberty is shown in some girls, leading to menorrhagia and irregular periods
Dental problems (caries, malocclusion, dysplastic, small teeth)
Visual impairment

Mechanism
The cause of this condition is unknown but evidence of familial inheritance and sporadic genetic mutation has been linked to cases of FHS. Two possibly familial cases have been reported—one in a mother and son, and the other in a mother and daughter. This suggests an autosomal dominant inheritance but additional cases need to be investigated to establish this. Another report has suggested that the inheritance may be autosomal recessive. In all of these cases, however, the mothers and children were not similarly affected, suggesting a variable clinical expression of the syndrome.In a study published by the American Journal of Human Genetics in 2012, exome sequencing was used to investigate a group of unrelated individuals with classic features of FHS and identified heterozygous mutations in SRCAP as causative of this disorder.
Each reported mutation was truncating (nonsense or frameshift) and occurred between codons 2,407 and 2,517 in exon 34, resulting in the loss of three C-terminal AT-hook motifs. SRCAP encodes a SNF2-related chromatin-remodeling ATPase that is a coactivator for CREB-binding protein (or CBP), which is the major cause of Rubinstein–Taybi syndrome. This disrupted interaction between the proteins most likely explains the clinical overlap between FHS and RTS. SRCAP has been shown to transduce signals of nuclear (steroid) hormone receptors and Notch pathways, showing that it plays diverse roles in gene expression. SRCAP contains several functional domains (SNF2 like ATPase, an N-terminal HSA domain, and three C-terminal AT-hook DNA-binding motifs). The CBP interaction domain of SRCAP is located centrally.Thus, the mechanism of disease in FHS is suspected to be dominant-negative (or antimorphic) due to the mutation in the final exon that results in the loss of the major transactivation function of SRCAP (or loss of one or more critical domains). All of the patients that carried the mutation also had obvious physical symptoms (i.e., prominent nose, delayed bone age, and short stature). Those who tested negative for the mutation often had dysmorphic facial features distinct from classical FHS, as well as a formal diagnosis of autism. Drawbacks to findings
From the same group, three individuals whose phenotype most closely resembled FHS carried no mutation on the SRCAP gene.