Therefore, melatonin is emerging as a promising mitigator of ER stress, demonstrating its potential to alleviate cellular stress and promote overall cellular survival across a spectrum of medical conditions.36, 37, 38 In our study, using Slc26a2-deficient chondrocytes induced by 4OH-Tamoxifen and an in vivo mouse model mimicking postnatal SLC26A2-deficient chondrodysplasia, we observed that melatonin successfully suppressed the expression of ER stress markers upon Slc26a2 deficiency. This evidence concerns the gene SLC26A2 and chondrodysplasia.