Using an epidermal lineage tracing approach in skin inflammatory mouse models with inducible epidermal deletion of c‐Jun and JunB, we show that mutant bulge hair follicle stem cells (HF‐SCs) are sufficient to initiate and maintain disease development, whereas mutant IFE cells, also initiators of the disease, are lost during psoriasis‐like progression. This evidence concerns the gene JUN and psoriasis.