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Thus, using immune checkpoint blockade (ICB) therapy to eradicate tumor cells will be more effective

In the absence of MTAP, the substrate methyl thionyl adenosine (MTA) accumulates and acts as a selective inhibitor of PRMT5 to inhibit PRMT5 methylation activity, 237 whereas MAT2A can produce the PRMT5 substrate SAM, 238 allowing PRMT5 to exert its oncogenic effect