ALG2, also known as apoptosis-linked gene 2 or PDCD6, has diverse functions. It is involved in processes such as protein sorting and export from endoplasmic reticulum exit sites (ERESs), innate immune responses, cell proliferation, migration, and tumorigenicity, as well as ovarian granulosa cell regulation and N -glycosylation [1-5, 7]. It is associated with pathways like the STING -mediated innate immune signaling pathway, the Wnt/β -catenin signaling pathway, and lysosome -dependent microautophagy pathway of ERESs. Genetic models are valuable for studying its functions.

In gene -knockout related studies, ALG2 knockout affected lysosome -dependent microautophagy of ERESs, preventing the engulfment of ERESs by lysosomes [1]. In THP -1 monocytes, ALG2 knockout increased the expression of type I interferons, suggesting its role in regulating STING -mediated innate immune responses [2]. In glioblastoma cells, down -regulation of ALG2 promoted cell proliferation, migration, and tumorigenic ability, indicating its tumor -suppressive role [3].

In conclusion, ALG2 is crucial in multiple biological processes. Studies using knockout models have revealed its significance in lysosome -related autophagy, innate immunity, and tumor -related processes. These findings contribute to understanding the mechanisms of related diseases, potentially providing new targets for treatment, such as in glioblastoma and congenital myasthenic syndromes where ALG2 mutations have been implicated [3,4,5].