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The mechanism by which CD38 mediated PD-1/PD-L1 blockade resistance likely includes perturbation of adenosine receptor signaling in tumor microenvironment leading to immune modulation (87)

The competition between NA methylation and NAD + salvage indicates that NNMT might limit fuel oxidation and promote fat storage, because if the activity or expression of NNMT is high, then, NA might not be salvageable, thus limiting the NAD + -dependent processes [16]

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