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These genotypes are associated with a myeloid-rich, T-cell-depleted immunosuppressive microenvironment resistant to PD-1/PD-L1 blockade [49, 393, 394]
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however, metabolic activities occurring in the mitochondria and endoplasmic reticulum and enzymes such as nicotinamide adenine dinucleotide phosphate (NADPH) oxidase are the usual causes associated with OS-mediated onset of T2DM (66) (Figure 1)
