(Top) Heat-shock protein H1 (HSPH1) binds to client proteins (CPs) involved in lymphomagenesis (eg, c-Myc, BCL-6) to generate a “mature complex” that contributes to the stabilization and maturation of those proteins, promoting their cellular function. (Bottom) HSP inhibitors would prevent binding of CPs to HSPH1, remaining in the cytosol, where CPs are ubiquitinated (Ub) and subsequently degradated by the proteasome.