In lung cancer-derived cells with exogenous overexpression of cancer-regulated gene 2 (CUG2), there is upregulation of EGFR and consequent resistance to doxorubicin treatment due to increased expression of antioxidant proteins such as MnSOD, Foxo1, and Foxo4 and the MDR genes MRP2 and BCRP. EGFR causes the activation of STAT1, a known factor of doxorubicin resistance, which was downregulated by the non-selective HDACs inhibitor TSA thanks to increased acetylation[68]. The gene discussed is EGFR; the disease is lung cancer.