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. This evidence concerns the gene EIF2AK3 and breast cancer.