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The complex multifactorial pathogenesis of acne vulgaris, the most common skin disease, may be explained at the level of genomic regulation. A recent hypothesis suggested that a relative nuclear defi ciency of the metabolic sensor and nuclear transcription factor FoxO1 appears to play a key role in the pathogenesis of acne vulgaris. FoxO1 has been identified as an important regulator of androgen receptor, cell proliferation, apoptosis, lipogenesis, oxidative stress regulation, innate and acquired immunity, all important aspects involved in the pathogenesis of acne. It is the intention of this review article to provide further evidence for the potential function of the PI3K/Akt/FoxO1 signaling pathway for other types of acne and acne-like eruptions.
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