Fntb, the farnesyltransferase β -subunit, is a key component of farnesyltransferase (FTase). FTase catalyzes the post-translational addition of a farnesyl group to proteins containing a CAAX motif, enabling these proteins to interact with cellular membranes. This process is involved in multiple cellular signaling pathways, such as those related to Ras proteins, which are crucial for cell growth, differentiation, and survival [5,6].

In Treg cells, Treg-specific deletion of Fntb leads to the development of fatal autoimmunity, indicating its importance in eTreg cell accumulation and function. Fntb promotes eTreg cell maintenance by regulating mTORC1 activity and ICOS expression [2]. In cardiomyocytes, overexpression of Fntb induces hypertrophy, apoptosis, and autophagic cell death, suggesting its role in cardiac remodeling and potential implications in heart-related diseases [3]. In breast cancer, certain Fntb promoter polymorphisms are independent predictors of survival, especially in triple-negative breast cancer (TNBC), and can modulate Fntb's transcriptional activity [1]. In ovarian cancer, the Fntb promoter polymorphism rs11623866 may be a potential predictive biomarker for lonafarnib treatment, as the G allele is associated with increased Fntb promoter activity and an unfavourable effect of lonafarnib is limited to patients with the GG genotype [4].

In conclusion, Fntb is essential for protein prenylation, which has far-reaching effects on various biological processes. Studies using gene-knockout or related models have revealed its significance in diseases such as autoimmunity, cardiac diseases, and certain cancers. Understanding Fntb's functions provides insights into the underlying mechanisms of these diseases and may guide the development of more targeted therapeutic strategies.