In this model of hypothyroidism, attenuation of the general transcription is not successful in maintaining the prosurvival environment into the cell, allowing the activation of proapoptotic pathways partially mediated by both PERK and ATF6 branches, since CREB2 and ATF6 induce the transcription of GADD153 [46] and this protein can activate cell death through several ways, including the repression of the Bcl2 gene and also the direct inhibition of Bcl-2, an antiapoptotic protein that binds proapoptotic proteins Bax and Bim and inhibits them [47]. Here, ATF6 is linked to hypothyroidism.