demonstrated LRRC8A‐E expression in multiple inner ear cell types using knock‐in mice.[34] Their study revealed that disruption of LRRC8A in the inner ear caused deafness with concomitant loss of Kir4.1 channels in stria vascularis and reduced endocochlear potential, suggesting VRAC's regulatory role in stria vascularis.[34] Additionally, Sox10Cre;Lrrc8afl/fl mice in Knecht's study exhibited earlier‐onset hearing loss (3 weeks).[34] This phenotypic divergence may stem from multicell LRRC8A ablation in their mice, where synergistic effects accelerate hearing loss progression. Here, KCNJ10 is linked to deafness.