Acne vulgaris (AV) is the most common skin disorder. It was traditionally thought that AV lesions developed after abnormal desquamation of the keratinocytes that line the sebaceous follicle, leading to hyperkeratinization and microcomedone formation. However, in recent years there has been a paradigm shift with regard to understanding the pathogenesis of AV, and it is now viewed as a primary inflammatory skin disorder. Research has implicated the presence of subclinical inflammation in the normal skin of acne patients, even before microcomedone formation. This article will review the novel concepts that play a role in the new pathogenesis of acne vulgaris.