The recruitment of effector CD8+ T cells into mouse flank skin via a viral infection (e.g. Vaccinia Virus) or through an inflammatory stimulus (e.g. “DNFB-pull”) results in comparable numbers of long-lived CD103+ epidermal TRM and is independent of the presence or absence of cognate antigen in the skin [18, 29, 31]. The gene discussed is CD8A; the disease is viral infectious disease.