Potential mechanisms contributing to increased cholesterol availability in cancer cell growth are believed to include tumor cells utilized cholesterol, uptake from the blood or de novo synthesis for membrane and lipid raft biosynthesis, and signaling molecules to facilitate their fast growth needs [41], while PCSK9 binds to the LDL-R to regulate lipoprotein homeostasis [8, 9] and immune checkpoints in cancer [42]. This evidence concerns the gene LDLR and neoplasm.