A new article published in Experimental Dermatology described seborrheic dermatitis (SD) as a very common chronic and/or relapsing inflammatory skin disorder whose pathophysiology remains poorly understood. Yeast of the genus Malassezia is deemed as a main predisposing factor for the disease, however, a causal relationship has not been firmly established. Additional predisposing factors have been described, including sebaceous activity, host immunity (especially HIV infection), epidermal barrier integrity, skin microbiota, endocrine and neurologic factors and environmental influences. Genetic studies in humans and animals implicate defects in the host immunity, epidermal barrier and sebaceous activity. Based on available evidence from literature searches, the authors proposed that intrinsic host factors, such as changes in the amount or composition of sebum and/or defective epidermal barrier, rather than Malassezia, may be the primary contributing factor to SD pathobiology. These intrinsic changes provide favorable conditions for the commensal Malassezia to over-colonize and elicit host inflammatory response. This article stated that aberrant host immune activity or failure to clear skin microbes may bypass the initial epidermal or sebaceous abnormalities. Thereafter, interactions of different epidermal compartments and immune components with the skin microbiota during the process of SD is said to influence the pathogenesis of the disease.