MST4-directed ATG4B phosphorylation at S383, but not at other described phosphorylation sites, contributes to increased autophagy activity, consequently facilitating tumorigenesis and drug resistance to RT in glioblastomas.169 Interestingly, ATG4B phosphorylation can also be independent of autophagic flux to perform tumorigenic functions. This evidence concerns the gene ATG4B and glioblastoma.