Another study conducted on γ-T3-treated MCF-7 and MDA-MB-231 breast cancer cells demonstrated an involvement of ER stress via both the PERK and inositol-requiring enzyme 1 (IRE1) pathways [69], leading to remarkable increment in their downstream targets, such as activating transcription factor 3 (ATF3) and CHOP, in response to γ-T3 treatment [69]. The gene discussed is ATF3; the disease is breast carcinoma.