Cholesterol, as a constituent of cell membranes, has a high activity in tumor cells, and to maintain cholesterol content in glioblastomas, the up-regulation of critical Autophagy genes, including ATG9B, ATG4A, LC3B, and NPC2, cause hydrolysis of cholesteryl esters in tumor cells to maintain cholesterol for tumor cell metabolism [72] (Fig. 3 and Table 1). This evidence concerns the gene MAP1LC3B and neoplasm.