Btg2, also known as PC3 or TIS21, belongs to the antiproliferative (APRO) gene family [3]. It acts as a tumor suppressor and is involved in numerous biological activities such as cell differentiation, proliferation, DNA damage repair, and apoptosis [3]. It is an immediate early response gene regulated by various factors and signaling pathways [3]. Also, it has been found to be related to maintaining T cell quiescence by promoting mRNA deadenylation and degradation [2].

In FSGS, podocyte-specific deletion of Btg2 protected against the onset of proteinuria and glomerulosclerosis in ADR-treated mice, inhibiting EMT markers and restoring epithelial markers [1]. This indicates Btg2 promotes FSGS via Smad3-dependent podocyte-mesenchymal transition [1]. In muscle stem cells (MuSCs), overexpression and knockdown of Btg2 in primary MuSCs respectively stimulated and prevented MuSCs senescence, suggesting Btg2 is a regulator of MuSC senescence [4].

In conclusion, Btg2 is crucial in multiple biological processes. Gene-knockout (KO) or conditional-knockout (CKO) mouse models have been instrumental in revealing its role in diseases like FSGS and muscle aging. These models help us understand that Btg2 can act as a regulator in disease-related cellular processes, providing potential therapeutic targets for these conditions.