Cytotoxic lymphocytes, including NK cells and cytotoxic T lymphocytes (CTLs), play a major role in the defense against neoplastic processes and viral infections (1). Granule exocytosis is the mechanism by which cytotoxic lymphocytes may induce lysis of its target. This involves granule-associated cytotoxic proteins, including the T-cell intracellular antigen-1 (TIA-1), perforin and granzyme B (1,2). Perforin produces pores that allow the entry of other cytotoxic proteins such as TIA-1 and granzymes, which trigger a process leading to DNA fragmentation and apoptosis of the target cells (1). However, there is evidence that granzyme B may kill targets independently of perforin (2). Recent studies (3,4,5) have demonstrated that the expression of granzyme B by immunohistochemistry in several entities of extranodal peripheral T cell lymphoma (PTCL) and NK cell lymphomas, including nasal and nasal-type NK/T cell lymphomas, hepatosplenic and non-hepatosplenic PTCL, enteropathy-type (ETCL) and non-ETCL intestinal PTCL, subcutaneous panniculitis-like PTCL (SPTCL), cutaneous CD8+ epidermotropic lymphomas as well as in nodal and cutaneous CD30+ anaplastic large cell lymphomas (ALCL) (3,4,5). In contrast, only a few nodal PTCL-unspecified (UC) express cytotoxic phenotype while angioimmunoblastic (AILD) lymphomas do not (3,4,5). The expression of cytotoxic proteins, such as granzyme B may be important for the identification and classification of extranodal T- and NK-cell lymphomas since many of these tumors do not have specific morphology and phenotype (6,7).