However, recent studies of non-neuronal cells demonstrated that (i) exposure of breast cancer cells to panobinostat (a pan HDAC inhibitor) led to deacetylation of GRP78, dissociation of GRP78 from PERK and increase the levels of pEIF2α, ATF4 and CHOP [32], (ii) exposure of colorectal carcinoma cells to tricostatin A (a pan-HDAC inhibitor) affected the binding of HDAC to GRP78 promotor [30] and (iii) the C-terminal region of RTN-C protein, an ER membrane protein, can interact with HDAC8 in vitro [50]. This evidence concerns the gene DDIT3 and breast cancer.