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There will be an emphasis on clinical findings in humans including additional syndromic findings that may aid in the diagnostic process.

Mouse models will be discussed as necessary to illustrate the components of these complex pathways.

However, genetic diagnosis of mutations affecting early gonadal development is becoming increasingly accessible to clinicians.

More powerful genetic techniques are allowing for interrogation of the entire genome for causative changes and it is important to be able to critically assess the flood of genetic data for meaningful information.

In this article, we aim to write a concise and clinically relevant review of genetic causes of 46, XX and 46, XY disorders of sex development (DSD) due to altered gonadal development.

The urethral folds differentiate into the penile urethra, glans, and corpus spongiosum in males and labia minora in females.

Androgen exposure and action are necessary for formation of male external genitalia and elongation of the phallus.

Within each category, the type of gonadal tissue is specified as testicular, ovarian, ovotesticular, or dysgenetic (streak).

The types of gonadal dysgenesis include complete, partial, and mixed.