In this study, Klotho mRNA expression was restored after treatment with 5-Aza, and histone deacetylation was also found to be a notable epigenetic silencing mechanism that could be reversed using the histone deacetylase inhibitor, trichostatin A. In the liposarcoma model, Klotho overexpression was observed to significantly decrease cell proliferation and clonogenicity, as well as increase apoptosis induced by cytotoxic ER stressors such as gemcitabine, thapsigargin, and the Bcl-2 inhibitor ABT-737 [75]. This evidence concerns the gene KL and liposarcoma.