Steroid users of teen age may find that their growth had been stunted by androgen and/or estrogen excess.

[17] Knockout-mice studies have shown that the androgen receptor is essential for normal female fertility, being required for development and full functionality of the ovarian follicles and ovulation, working through both intra-ovarian and neuroendocrine mechanisms.

Experimental data using AR knockout female mice, provides evidence that the promotion of cardiac growth, kidney hypertrophy, cortical bone growth and regulation of trabecular bone structure is a result of DNA-binding-dependent actions of the AR in females.

[citation needed] The primary mechanism of action for androgen receptors is direct regulation of gene transcription.

[20] This androgen response mechanism is perhaps best known and characterized in the context of male sexual differentiation and puberty, but plays a role in a variety of tissue types and processes.

[24] Androgen receptors interact with other proteins in the nucleus, resulting in up- or down-regulation of specific gene transcription.

[25] Up-regulation or activation of transcription results in increased synthesis of messenger RNA, which, in turn, is translated by ribosomes to produce specific proteins.

One function of androgen receptor that is independent of direct binding to its target DNA sequence is facilitated by recruitment via other DNA-binding proteins.

[27] Androgen receptor is modified by post-translational modification through acetylation,[28] which directly promotes AR-mediated transactivation, apoptosis[29] and contact-independent growth of prostate cancer cells.

[32] The AR acetylation site is a key target of NAD-dependent and TSA-dependent histone deacetylases[33] and long non-coding RNA.

[43] The racial trends in CAG repeats parallels the incidence and mortality of prostate cancer in these two groups.