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In this study, we attempted to ascertain whether the other members of the GST family, particularly those belonging to the GSTM group, can compensate for the loss of the GSTM1 enzyme due to the absence of GSTM1 under normal physiological conditions

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We posit that further analyses of additional mouse models of endometriosis with specific lesion genotypic aberrancies, in the context of specific diets, may improve current understanding of genetic and environmental interplay in this condition

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