For example, although deletion of PERK attenuates Neu-dependent mammary tumor progression and lung metastasis, long-term PERK inactivation promotes spontaneous mammary tumorigenesis owing to increased genomic instability.59 PERK activation also contributes to MYC-induced cell transformation and tumorigenesis through autophagy.60 This may be related to PERK-mediated eIF2α phosphorylation, resulting in increases of the levels of ATF4, CHOP, and factors that activate the transcription of many autophagy genes. Here, DDIT3 is linked to breast cancer.