In general, pharmacological inhibition of critical protein kinases acting upstream of MYC could lead to reduced MYC expression by depleting oncogenic survival signals, as shown previously by simultaneous activation of PP2A and inhibition of mTOR in pancreatic adenocarcinoma (92), also demonstrating that the PI3K/AKT/mTOR pathway inhibition exhibits therapeutic activity in distinct MYC-driven cancers (22). The gene discussed is MYC; the disease is pancreatic adenocarcinoma.