It has been reported that the low or absence of VPS4B makes cells more dependent on VPS4A.[8] Intriguingly, the Cancer Genome Atlas (TCGA) and Clinical Proteomic Tumor Analysis Consortium (CPTAC) database showed that the mRNA and protein level of VPS4B in tumor tissues of patients with LUAD was significantly lower than normal tissues (Figure S11A,B, Supporting Information). This evidence concerns the gene VPS4B and neoplasm.