In the pro‐oncogenic aspect, hypercholesterolemia and hypertriglyceridemia can intensify inflammation and oxidative stress, fostering a mutagenic inflammatory microenvironment and excessive ROS/RNS, thereby leading to DNA damage, activating proto‐oncogenes (e.g., Ras) and suppressing tumor suppressor genes (e.g., P53) [6]. This evidence concerns the gene TP53 and Hypercholesterolemia.