Recent in silico studies indicate that ATG5 splice-site mutations that trigger exon skipping or introduction of a frameshift that might prevent ATG5 expression, are found in multiple tumor types, among them, cervical squamous cell carcinoma (exon 2 skipping), hepatocellular carcinoma (exon 3, 6 or 7 skipping) or uterine corpus endometrial carcinoma (exons 4 and 7 skipping), suggesting that alterations in ATG5 mRNA splicing may not be limited to some prostate cancer cells92. Here, ATG5 is linked to prostate cancer.