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However, they found that in knock-in mice expressing MOR mutant S375A substitution, proposed by these authors to be the primary site of morphine-induced phosphorylation of MOR responsible for desensitization (Schulz et al., 2004), morphine tolerance was not affected (Grecksch et al., 1999) cannot be extended to DOR

HBGVs should ideally be derived from human epidemiological data or be determined based on in vivo animal studies

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This assumption is supported by the finding that only the overexpression of GCL, and not of GS, results in increased GSH levels (6)