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We demonstrate that: (1) SC-specific GSDMD deletion protects against NIHL, (2) noise-induced oxidative stress in HCs triggers a signaling cascade via epidermal growth factor receptor/extracellular-regulated kinases (EGFR/ERK), which activates caspase-11-dependent GSDMD cleavage in SCs

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A higher concentration means fewer units are needed for the same milligram dose

Together, these findings provide direct evidence that high MYC expression plays a causal role in repressing pRB1 abundance via proteasomal degradation

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