In recent studies, D’Abronzo and colleagues discovered that elevated phosphorylated eIF4E (p-eIF4E) levels induced by antiandrogen bicalutamide (Figure 1) rendered prostate cancer cells in tumor xenografts and clinical tumors resistant to antiandrogen/mTORC1-inhibitor treatment [19], suggesting that targeting of Mnk1/2 signaling may be a critical adjunct for effective treatment of prostate cancer [9,11,20,21,22]. The gene discussed is EIF4E; the disease is neoplasm.