The association between the ER stress response and the autophagic flux induced by vemurafenib was further confirmed using the PERK inhibitor, GSK2606414, where the ratio of LC3II/LC3I was reduced, together with suppression of p62/SQSM1 digestion and reduced CHOP levels, suggesting that the ER stress response plays a crucial role in inducing autophagy during vemurafenib treatment in thyroid cancer; these findings mirror those of Ma et al. [27] in the melanoma model. The gene discussed is SQSTM1; the disease is thyroid gland carcinoma.