Iwasa and colleagues’ use of the Woodchuck Hepatitis Virus post-transcriptional regulatory element (WPRE) to augment Tmc1 transgene expression resulted in poor hearing recovery [55], and found that Tmc1 expression in OHCs was higher in animals treated with WPRE-containing vectors than in the group without WPRE by scRNA-seq analysis, with a relatively better therapeutic efficacy, suggesting that optimizing the dose of the transgene expressed in the target cells is essential for gene therapy for hearing loss. This evidence concerns the gene TMC1 and hearing loss disorder.