result in an individual that can be identified as a mosaic strictly based on phenotype. mosaicism also results from a phenomenon known as x-inactivation. all female mammals have two x chromosomes. to prevent lethal gene dosage problems, one of these chromosomes is inactivated following fertilization. this process occurs randomly for all of the cells in the organism's body. because a given female's two x chromosomes will almost certainly differ in their specific pattern of alleles, this will result in differing cell phenotypes depending on which chromosome is silenced. calico cats, which are almost all female, demonstrate one of the most commonly observed manifestations of this process. trinucleotide repeat disorders main article: trinucleotide repeat disorder trinucleotide repeat disorders also follow a non-mendelian pattern of inheritance. these diseases are all caused by the expansion of microsatellite tandem repeats consisting of a stretch of three nucleotides. typically in individuals, the number of repeated units is relatively low. with each successive generation, there is a chance that the number of repeats will expand. as this occurs, progeny can progress to premutation and ultimately affected status. individuals with a number of repeats that falls in the premutation range have a good chance of having affected children. those who progress to affected status will exhibit symptoms of their particular disease. prominent trinucleotide repeat disorders include fragile x syndrome and huntington's disease. in the case of fragile x syndrome it is thought that the symptoms result from the increased methylation and accompanying reduced expression of the fragile x intellectual disability gene in individuals with a sufficient number of repeats.