By introducing a panel GLuc reporters for 12 cancer-associated pathways as described [40,41], along with a constitutively active reporter pG2Luc, we found that three pathways, containing ElK1, Ap1 and Myc/max, were significantly attenuated in RKO cells exposed to either 2 μM or 4 μM of monensin at 48 h post-treatment (p < 0.05, Figure 5(A)). The gene discussed is MYC; the disease is cancer.