We targeted TAM67 to the suprabasal epidermis to inhibit AP1 factor-related transcription in this compartment.4, 5 Our findings show that TAM67-dependent inactivation of AP1 factor function in the suprabasal epidermis results in increased cell proliferation and delayed differentiation and that this is associated with extensive epidermal hyperkeratosis and formation of constriction rings on the tail and digits5 to produce a phenotype that resembles human keratoderma.4, 5. The gene discussed is JUN; the disease is Hyperkeratosis.