T cell large granular lymphocytic leukaemia is a chronic, T cell lymphoproliferative disorder which characteristically demonstrates a clonal proliferation of mature, cytotoxic T cells. Additionally designated as T cell large granular lymphocytosis or T cell lymphoproliferative disease of granular lymphocytes, T cell large granular lymphocytic leukaemia is associated with diverse autoimmune disorders. Generally, neoplastic CD8+ T lymphocytes appear immune reactive to NK cell immune markers. An estimated (50%) subjects manifest a STAT3 / STAT5b genetic mutation. Of obscure aetiology, the indolent T cell large granular lymphocytic leukaemia is commonly associated with mono-cellular, bi-cellular or pancytopenia. Emerging neutropenia or anaemia mandates commencement of cogent therapy. T cell large granular lymphocytic leukaemia configures up to 5% of mature lymphocytic leukaemia and preponderantly incriminates peripheral blood, bone marrow, spleen or hepatic parenchyma. Characteristically, bone marrow, spleen or hepatic parenchyma exhibits an intra-sinusoidal pattern of tumour cell dissemination. T cell large granular lymphocytic leukaemia is frequently encountered within elderly individuals with median age of disease emergence at 60 years. An equivalent gender predisposition is observed [1,2]. T cell large granular lymphocytic leukaemia represents with oligo-clonal expansion of cytotoxic large granular T cells occurring as a consequence to antigenic stimulation. Subsequently, clonal proliferation of large granular T cells ensues on account of constitutive upregulation of signals of cellular survival accompanied by downregulation of apoptotic pathways through a secondary genetic manifestation [1,2]. Generally, genomic mutations of STAT3 or STAT5b may emerge as a secondary event. Besides, resistance to Fas / FasL mediated cellular mortality, enhanced cellular survival on account of interleukin 15 (IL15) and platelet derived growth factor (PDGF) associated with activation of nuclear factor kappa-light- chain enhancer of activated B cells (NFkB) pathway may configure as inducing secondary manifestations. Neutropenia and anaemia may occur due to direct cytotoxicity engendered from monoclonal, neoplastic T lymphocytes.