 A study conducted in children demonstrated an association between GSTM1 and GSTT1 polymorphisms presence of at least one null genotype and the development of grade 3 or higher toxicity related to treatment of medulloblastoma. However, this study, based on a small sample of children 42 children, 19 of whom experienced severe ototoxicity and comprising patients receiving very different treatments, was unable to determine the proportion of toxicity specifically related to platinum derivatives, as some patients also received brain irradiation. Furthermore, this association between GST polymorphisms and toxicity was not observed when the analysis was specifically confined to grade 3 or higher ototoxicity. Finally, the role of GSTP1 Ile105Val polymorphism has not been evaluated in children Barahmani et al., 2009. To our knowledge, only one study has specifically evaluated the potential impact of GST polymorphism on cisplatin ototoxicity in children. This study showed a protective effect of the GSTM3B variant, but did not observe a protective effect of the GSTP1 105Val allele with respect to ototoxicity, as demonstrated in adults for neurotoxicity. However, these findings were based on small sample sizes 20 patients with ototoxicity versus 19 patients without ototoxicity and the ototoxicity experienced by these patients was grade 2 8 patients or 3 12 patients with no cases of grade 4 ototoxicity Peters et al., 2000. The results of this study therefore need to be confirmed by a study comprising a greater number of patients, cases and controls, including patients with more severe ototoxicity. Ross et al., studying drug metabolism enzymes, demonstrated a highly significant association between cisplatin ototoxicity in children and genetic variants of TPMT rs12201199, p 0.00022, OR 17.0 and COMT rs9332377, p 0.00018, OR 5.5. However, as the role of these enzymes in detoxification of platinum derivatives has not been previously reported, these results need to be confirmed by other studies with, in particular, matching for age, exclusion of cases of grade 2 ototoxicity from the group of severe ototoxicity, and a greater number of control patients Ross et al., 2009. Finally, no study has investigated the genetic factors involved in carboplatin ototoxicity in children. One study concerning membrane transporters showed that a common polymorphism situated in the promoter region of the MRP2 -24CT transporter gene was associated with a better response to platinum-based chemotherapy allelic frequency: 18 of Caucasian Cascorbi, 2006; Sun et al., 2009. It would be interesting to determine whether polymorphisms affecting this gene can also modulate the toxicity of these treatments. A polymorphism of the gene coding for the influx transporter OCT2 c.808GT; p.270AlaSer has also been shown to be associated in vivo and in vitro in mice with a protective effect in relation to cisplatin nephrotoxicity and ototoxicity Ciarimboli et al.; Filipski et al., 2009, but the potential influence of this polymorphism on platinum ototoxicity has never been demonstrated in man. It therefore appears very interesting to study the potential impact of this polymorphism in the context of our study. 