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Complete gonadal dysgenesis (CGD) is characterized by bilateral dysgenetic gonads, intact Müllerian duct derivatives, and external female phenotype with either 46, XX or 46, XY karyotype.

Partial gonadal dysgenesis (PGD) refers to a 46, XY individual with partial testicular differentiation, some internal Müllerian derivatives, and ambiguous external genitalia.

The dosage-dependence of genes involved in gonadal development is a recurrent theme, and genetic changes in promoter and repressor regions are being revealed by chromosomal microarray analysis and other techniques.Production of testosterone by Leydig cells promotes development of the mesonephric or Wolffian ducts, which develop into the epididymis, vas deferens, and seminal vesicles.The Müllerian ducts become the fallopian tubes, uterus, and upper two-thirds of the vagina.In some cases, there are multiple different phenotypes caused by deletion, duplication, homozygous, heterozygous, and regulatory-region changes in the same gene.We aim to provide a concise and clinically-applicable overview of recent developments in the understanding of DSD caused by genetic changes affecting gonadal development.