Furthermore, a recent mice model study suggested a complex pathogenesis of thyroid dysfunction in cystinosis, including accelerated thyrocyte turnover, increased cell proliferation, enhanced apoptosis linked to endoplasmic reticulum stress, impaired thyroglobulin production, and altered endolysosomal trafficking and iodothyroglobulin processing [25], further emphasizing apoptosis as a contributing factor to thyroid dysfunction in cystinosis, which supports our hypothesis. Here, TG is linked to cystinosis.