The concept that acne vulgaris might be induced by a genuine inflammatory sebocyte response, first published in 2001 (88) obtained partial confirmation in 2003 through the detection of CD3+, CD4+ T cells in the perifollicular dermis of acne microcomedones before even the initiation of sebocyte and follicular keratinocyte hyperproliferation, associated with the acne lesions (89). The gene discussed is CD4; the disease is acne.