**2. Polymorphisms at DNA level**

Genomic variability at DNA level can be present in many forms including: single nucleotide polymorphisms, variable number of tandem repeats (e.g., mini- and microsatellites), transposable elements (e.g., Alu repeats), structural alterations, and copy number variations. It can occur in the nucleus or mitochondria. Two major sources: (1) mutations that may result as chance processes or have been induced by external agents such as radiation and (2) recombination. Once formed, it can be inherited, allowing its inheritance to be tracked from parent to child [3].

The genomes of humans may be divided into different parts based on known functional properties; the coding and noncoding regions mostly do not code for protein [2, 9]. The coding regions contain DNA sequences which determine primarily the amino acid sequences of the proteins for which they code. Noncoding DNA generally containing DNA sequences with no function has not yet been discovered or possibly no function exists [10]; such sequences may be either single copy or exist as multiple copies called repetitive DNA [10]. Indeed, regions of DNA that do not code for proteins tend to have more polymorphisms. Recently, there has been substantial progress in understanding genome content which centered on discovered protein-coding genes which considered a functional DNA sequence moving away for discoveries of many repeat families, and various copy number variations encompass gene copies leading to dosage imbalance that plays an important role in genome structure, evolution, and diversity [11, 12]. "The Human Genome Project has revealed that humans have only 20,000–30,000 structural genes (protein-coding genes) (International Human Genome Sequencing Consortium, 2004)" [13].
