In our study, we observed that the endogenous LC3 puncta were significantly increased in both HCs and HC-like HEI-OC1 cells after Dync1li1 KO or KD, which suggested that without dynein the process of autophagosome clearance was abnormal and that this led to the accumulation of autophagosomes in HCs that in turn triggered apoptosis in HCs and subsequent hearing loss. The gene discussed is MAP1LC3A; the disease is hearing loss disorder.