Psoriasis is a chronic inflammatory skin disease characterized by periods of remission and relapse. In this pathology, keratinocytes, dendritic cells, and different subpopulations of T cells are critical to developing psoriatic lesions. Although current treatments can reduce symptoms, they reappear in previously injured areas months after stopping treatment. Evidence has pointed out that besides T-helper 17 cells, other T-cell subsets may be involved in relapses. This review focuses on the leading evidence linking resident memory T cells and P2X7 receptor to psoriasis' pathogenesis and their role in this pathology. Finally, we discuss some of the most widely used experimental murine models and novel strategies to investigate further the role of resident memory T cells in psoriasis.