The cause of atopic dermatitis is complex and primarily genetically determined, although environmental co-factors play a role. It is characterized by barrier dysfunction but particularly filaggrin gene mutations. The skin in atopic dermatitis is highly colonised by Staphylococcus aureus and other staphylococcal species which exist on dry skin zones in mild, as well as in severe disease manifestations. The role of staphylococci has been elusive until now. However, the current hypothesis is that staphyloccoccal antigens are thought to act as super-antigens causing non-specific symptom exacerbation. Therefore, increased staphylococci colonization/infection could be responsible for flares. Reducing bacterial load will result in clinical improvement. The human microbiome (from the Greek micro "small" and bios "life") is a "living organism" existing on various bodily surfaces. The cutaneous microbiome is an ecosystem composed of trillions of microorganisms (bacteria, yeast, viruses, fungi etc.) which colonise the stratum corneum. Recently, it was shown that the microbiome or biofilm differs from normal skin in atopic dermatitis, and psoriasis. In atopic dermatitis that is the case for involved and non-involved skin. Staphylococci form a biofilm thus playing a dominant role in the occluding sweat ducts, leading to inflammation and pruritus. This may also explain why regular baths of diluted bleach (sodium hypochlorite) and intranasal application of mupirocin ointment reduces the disease severity in both children and adults, in particular with secondarily infected eczema. Severe childhood atopic dermatitis has been show to be successfully treated with wet wraps ("wet pyjama") and diluted corticosteroids but also with antiseptics and therefore indirectly supporting the role of the microbiome. A next step will be the development of emollients with antibacterial activities, that will restore a balanced microbiome in the damaged atopic skin and respect normal skin microbiome. Currently such products are on the market.