Within this context, potential inhibitory therapeutic strategies could include: siRNA inhibition of MCPyV large T antigen expression to prevent alternative TrkAIII splicing; siRNA and PNA inhibitors of TrkAIII expression, reported to enhance the sensitivity of TrkAIII expressing cancer cells to cytotoxic agents; TRAIL, reported to induce apoptosis in TrkAIII expressing neuroblastoma cells, and cell-permeable small molecule TrkA inhibitors, reported to inhibit TrkAIII activity and sensitize TrkAIII expressing cancer cells to cytotoxic agents [19–25, 40]. The gene discussed is TNFSF10; the disease is cancer.