Lipg, also known as endothelial lipase (EL), is a gene with crucial functions in the human body. It predominantly acts as a phospholipase and also exhibits low levels of triglyceride lipase activity. It plays an essential role in lipoprotein metabolism and is involved in metabolic syndromes such as the inflammatory response and atherosclerosis [1].

In breast cancer, studies have shown that the risk of breast cancer increases with higher levels of LIPG, especially in pre-menopausal, Luminal A, HER2-negative, non-postpartum, and grades II and III breast cancers [2]. LIPG-promoted lipid storage in breast cancer cells mediates adaptation to oxidative stress, which supports tumor progression [3].

In lung adenocarcinoma, LIPG expression is higher in tumor tissues, especially in certain subgroups, and is associated with a poor prognosis, lipid metabolism, and immune infiltration [4].

In colorectal cancer, ZDHHC1 downregulates LIPG to inhibit cancer cell growth [5].

In human basal-like triple-negative breast cancer, LIPG is overexpressed and is required for tumorigenicity and metastasis, and its phospholipase activity is related to tumor formation [6,7].

Additionally, in the Maonan and Han nationalities in China, certain LIPG SNPs and their haplotypes are associated with serum lipid levels [8].

In conclusion, Lipg is involved in various biological processes, especially in lipid metabolism. Its abnormal expression is closely related to multiple cancers, including breast, lung, and colorectal cancers. The study of Lipg using gene-knockout or conditional-knockout mouse models (although not explicitly mentioned in all references but inferred as a valuable approach) can help further understand its role in these diseases, providing potential directions for targeted therapies.