Notably, three of the four proteins that helps activate the T-cell receptor (TCR) in the TCR complex CD3E (CD3ε), CD247 (CD3ζ) and CD3D (CD3δ) were among the ten most downregulated (1.9-fold) in Jurkat following SAHA treatment (Table 2), in agreement with earlier findings [35] and may explain the mono-therapy effects of HDACis in peripheral T-cell lymphomas such as CTCL, where T cell receptor activation can be a sustaining factor [36]. The gene discussed is CD3D; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.