Consistent with the tumor-promoting role of tNOX suggested by many previous studies, oxaliplatin-treated MKN45 and TMK-1 cells showed no down-regulation of tNOX at both translational and transcriptional levels (in fact, some up-regulation of tNOX was observed in TMK-1 cells), increased expression of survivin (an anti-apoptotic factor), and no evidence of caspase 3-directed PARP cleavage (Figure 4C). The gene discussed is CASP3; the disease is neoplasm.