Zappasodi and colleagues demonstrated that inactivation of HSP105/HSPH1 leads to downregulation of c-Myc and Bcl-6 (120).Mechanistically, HSP105 showed to interact with c-Myc and Bcl-6 in nucleus in primary human DLBCL and BL cells, suggesting that HSP105 may function as a chaperone for both c-Myc and Bcl-6 (120).Additionally, higher expression of HSP105 was found in DLBCL expressing c-Myc compared to c-Myc low/negative counterparts (120). The gene discussed is BCL6; the disease is Burkitt lymphoma.