STAT3 and cholangiocarcinoma: To corroborate whether or not these mechanisms are in fact involved in modulating STAT3 pathway activity in cholangiocarcinoma cells upon administration of EF24, SNU478 and HuCC-T1 cells were pretreated with either 10 mM N-acetyl cysteine (NAC), a precursor to GSH, or a cell permeable glutathione monoethyl ester (GEE; c = 10 mM), which is cleaved to GSH intracellularly, for 2 hours and thereafter with 2.5 μM EF24 for another 6 hours (Figure 6(c)).