MYC occupies the promoters of lysosome and ATGs, resulting in TFEB, TFE3, and FOXH1 promoter dissociation.90 As a classic tumor inducer, MYC is frequently overexpressed and genetically mutated in numerous human cancers.92 Therefore, it is likely to support the notion that tumors rely on the HDAC/MYC-TF axis to sustain proliferation and growth by repressing autophagic and lysosomal systems. Here, MYC is linked to neoplasm.