Myopia, or nearsightedness, results from a mismatch between the axial length of the eye and the refractive power. Severe (high) myopia increases the risk of other eye conditions like glaucoma and can be caused by frameshift mutations in the LRPAP1 gene. However, the mechanism of LRPAP1-related high myopia isn’t clear. To learn more, researchers recently investigated the effects of an LRPAP1 frameshift mutation on refractive development in zebrafish. The mutant zebrafish showed a myopic phenotype, with greater axis length/body length ratios than the wild-type fish beginning at one month of age. The relative refractive error values were also shifted in the mutant fish starting at two months and the collagen fibers in these fish thinned and became disordered. Furthermore, apoptosis was activated in the mutant zebrafish, and the proapoptotic protein TGF-β was upregulate, but TGF-β inhibitor treatment attenuated the mutation-induced apoptosis. Although the related molecular changes need clarification, the findings reveal that LRPAP1 mutation may cause myopia via TGF-β-induced apoptosis, bringing a potential mechanism of high myopia into focus.