ATG16L1 and neoplasm: Having identified an ATG5 splice site mutation in DU145 PCa cells that resulted in the loss of ATG5, ATG12, and ATG16L1 protein expression and the inactivation of autophagy, we next questioned whether other tumors might possess similar splice site mutations that impair mRNA splicing of ATG5. We searched human tumor mutation databases and found several unique ATG5 splice site mutations identified in multiple tumor types.