Vnn3, also known as vanin-3, is a member of the pantetheinase gene family. Pantetheinase enzymes hydrolyze pantetheine into pantothenic acid and cysteamine, with cysteamine being a key regulator of host responses to inflammatory stimuli [4,5].

Vnn3 has been associated with multiple disease conditions. In clear cell renal cell carcinoma (ccRCC), high Vnn3 expression is linked to poor prognoses, making it a potential biomarker for predicting ccRCC prognosis [1]. In benzene-exposed workers, Vnn3 expression is correlated with hemogram and influences cell proliferation induced by 1,4-benzoquinone, a benzene metabolite, by regulating KLF15 and NOTCH1 expression, suggesting it could be a biomarker of benzene toxicity [2]. In heart failure, Vnn3 is one of the four identified diagnostic markers associated with neutrophil extracellular traps (NETs), enhancing the understanding of immunology in heart failure [3]. Mice defective in Vnn3 show increased susceptibility to blood-stage malaria, and supplementation with cysteamine corrects part of the malaria-susceptibility phenotype, indicating Vnn3's role in host response to malaria [6]. In chronic heart failure patients, Vnn3 is independently associated with an elevated neutrophil-to-lymphocyte ratio (NLR), which may help in prognosis prediction [7].

In conclusion, Vnn3 is involved in various biological processes related to disease, such as cancer prognosis, response to chemical toxicity, immunology in heart failure, and host response to malaria. Studies on Vnn3-deficient mouse models have provided valuable insights into its role in these disease areas, contributing to a better understanding of disease mechanisms and potential biomarker discovery.