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The defensin-related pseudogenes show premature stop codons, have start-codon mutations or miss different conserved amino acids

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The findings revealed that the methylation of genes associated with mitochondria was dramatically decreased, indicating impaired mitochondrial function

However, the invasive method and high mortality rate are two drawbacks of this model

[3] and our observations [10, 11] may soon guide the development of novel and relevant clinical studies that aim to increase the knowledge of G6PD deficiency and explore the clinical relevance of the relationship of G6PD-deficient variants with the pathophysiology of CVD