Lichen planus is a chronic inflammatory mucocutaneous disorder commonly affecting the skin, nails, hair, and mucous membranes (1). Although its main cause is still unclear, lichen planus is defined as a T cell- mediated inflammatory disease (2). CD8+ T lymphocytes activate their cytotoxic armamentarium and induce basal keratinocyte apoptosis (2). The susceptibility of basal keratinocytes to CD8+ T lymphocytes is enhanced through MHC class I expression on keratinocytes triggered by interferon (IFN)- gamma (3). The cytotoxic process is mainly mediated by the release of lytic molecules, such as perforin, granzyme B, and granulysin (GNLY) (4–8). The upregulation of perforin and granzyme B has been previously demonstrated in the peripheral blood and lesional skin of patients with lichen planus (4–8). GNLY is a member of the saposin-like lipid-binding protein (SAPLIP) family and has a cytotoxic effect on tumour cells and a variety of microorganisms (9, 10). It is located in the cytotoxic granules of T cells, which are released upon antigen stimulation, and in the cytotoxic granules of natural killer (NK) cells. GNLY presence has only recently been observed in lichen planus lesions, but the expression level of this molecule in peripheral blood and subsequent determination of cells that express this molecule in blood and lesions remains unknown (8). In this study we examined the dynamics of GNLY expression in different cytotoxic subtypes of peripheral blood lymphocytes and in the skin lesions of patients with lichen planus.