BCL2 and hypothyroidism: Impaired redox status concomitant with sustained ER stress, as well as a plethora of the misfolded protein aggregates relevant to hypothyroidism, provoked cascades of neuronal death (Blas-Valdivia et al. 2021; Shi et al. 2022) that was obviously seen by the overexpression of the apoptotic markers (CHOP, Bax, and caspase-12) along with the suppression of the anti-apoptotic Bcl2 protein in the brain of the hypothyroid rats.