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. Author manuscript; available in PMC: 2021 Aug 17.
Published in final edited form as: Leukemia. 2019 Oct 17;34(3):957–962. doi: 10.1038/s41375-019-0601-y

Fig. 2.

Fig. 2

Pathogenesis model for LGL leukemia. Activation resulting in the oligoclonal/purely clonal cytotoxic T cell expansion. a LGL coexistent theory confers to the development of clonopathies and persistence as the result of age-related changes. LGL may coexist with ICUS, BCUS, MGUS, CHIP, and TCUS. b, c Pressured evolution theory, however, suggests that LGL evolution is either the result of myeloid aberrancies or may indeed be the cause of myeloid aberrancy occurrence. Further, LGL may play an integral role in either (1) Eradicating or (2) Controlling the aberrancy or completely failing to harness the escape clone leading to disease advancement to MDS. d Fate of precursor (myeloid and erythroid) and hematopoietic stem cells (Normal and MDS) when targeted by LGL and the associated clinic-pathological conditions