Similarly, the decrease in LAG3 suggests that this checkpoint is not a limiting factor for the therapeutic efficacy of this treatment; however, the significant increase in TIM3 supports the possibility that upregulation of it or similar, alternative checkpoints may be responsible for maintaining an immunosuppressive environment and dampening the anti-cancer immune response after combined inhibition of PD-1 and CTLA-4. The gene discussed is CTLA4; the disease is cancer.