TMEM106B and neoplasm: Newman et al[20] found that TRAF3IP3 can upregulate the TGF-β signaling pathway, promote cellular autophagy, and activate CD40 to activate the immune response by promoting NFκB activated.[21,22] Similarly, TM6SF1, NEU1, NPRL2, and TMEM106B, as key genes for lysosome formation, could enhance lysosomal function and thus further regulate tumor progression.[23,24] Epithelial mesenchymal transition (EMT), a crucial stage in building the tumor microenvironment, plays an integral part in the progression of LUAD.