91–96% demonstrate inattention, 75% impulsivity, 59–71% hyperactivity 46–74% tantrums, 32–60% disobedience, and 25–37% fighting and aggressive behavior.In one experiment, a group of children with Williams syndrome showed no signs of racial bias, unlike children without the syndrome. They did show gender bias, however, to a similar degree to children without the syndrome, suggesting separate mechanisms for these biases. Cause
Williams syndrome is a microdeletion syndrome caused by the spontaneous deletion of genetic material from the chromosomal region 7q11.23. This is a hemizygous deletion, which results in haploinsufficient expression of the 25–27 genes in this region. CLIP2, ELN, GTF2I, GTF2IRD1, and LIMK1 are among the genes typically deleted. Hemizygosity for the ELN gene, which codes for the extracellular matrix protein elastin, is associated with connective-tissue abnormalities and cardiovascular disease (specifically supravalvular aortic stenosis and supravalvular pulmonary stenosis). Elastin insufficiency may also contribute to distinct faces, harsh or hoarse voice, hernias, and bladder diverticula often found in those with Williams syndrome. Hemizygosity in LIMK1, GTF2I, GTF2IRD1, and perhaps other genes may help explain the characteristic difficulties with visual–spatial tasks. Additionally, some evidence shows that the hemizygosity in several of these genes, including CLIP2, may contribute to the unique behavioral characteristics, learning disabilities, and other cognitive difficulties seen in WS. Diagnosis
According to the Williams Syndrome Association, its diagnosis begins with the recognition of physical symptoms and markers, which is followed by a confirmatory genetic test.
Keratosis follicularis may refer to:

Dariers disease
Focal palmoplantar keratoderma with oral mucosal hyperkeratosisSee also:

Isolated dyskeratosis follicularis
Keratosis follicularis spinulosa decalvans