The fact that ATG5 is selectively inactivated by somatic mutations and/or alternative mRNA splicing (Figs. 1 and 3), and that ATG16L2 is transcriptionally overexpressed, relative to ATG16L1, in multiple tumor types (Fig. 5g), suggests that the inhibition of autophagy is indeed oncogenic. This evidence concerns the gene ATG5 and neoplasm.