Recent evidence suggests that fibrosis may play an important role in the pathobiology of rhinophyma. The fibrogenic cytokine transforming growth factor (TGF)-beta2 has been reported to be up-regulated in rhinophyma tissue. Of the three common isoforms of TGF-beta, TGF-beta1 and TGF-beta2 are considered fibrogenic, whereas TGF-beta3 has antiscarring properties. To provide further evidence for the role of fibrosis in the pathobiology of rhinophyma, specimens from 8 patients with rhinophyma were compared with nine specimens of normal nasal skin. Immunohistochemistry was used to compare intensity levels of TGFbeta1 and TGFbeta3 proteins, and quantitative reverse transcription-polymerase chain reaction was used to determine messenger ribonucleic acid (mRNA) expression levels of TGFbeta1 and TGFbeta3. TGF-beta1 was elevated significantly in rhinophyma tissue (p < 0.001), whereas TGF-beta3 was no different in the rhinophyma specimens compared with normal nasal skin (p = 0.06). TGFbeta1 mRNA expression was five-fold higher in rhinophyma tissue compared with normal skin (p < 0.001). The mRNA expression of TGF-beta3 was the same for both pathological and normal tissue (p < 0.09). These data, together with previously published observations, present further evidence that fibrosis mediated by the fibrogenic cytokines TGFbeta1 and TGFbeta2 play a role in the pathobiology of rhinophyma and suggest a means of treatment by neutralizing or down-regulating these cytokines.