Rgs16, the regulator of G protein signaling 16, is involved in regulating G protein-coupled receptor signal transduction pathways. It plays a significant role in various biological processes and is associated with multiple diseases [3].

In cancer, Rgs16 has diverse impacts. In tumors, it promotes antitumor CD8+ T cell exhaustion by suppressing Tex cell survival. Rgs16-deficient CD8+ T cells show inhibited apoptosis and enhanced antitumor effector functions, and its deficiency synergizes with PD-1 blockade [1]. In esophageal cancer, Rgs16 promotes cell proliferation and migration by regulating Hippo-YAP activity [2]. In glioma, it is upregulated, promotes progression, and serves as an independent prognostic factor [4,5].

In liver injury related to HBV infection, HBeAg upregulates Rgs16 expression, which then enhances macrophage activation and accelerates liver injury through ERK phosphorylation [8].

In ulcerative colitis, Rgs16 expression in the colonic mucosa and PBMCs is increased and correlated with disease activity, suggesting it as a potential therapeutic marker [6].

In schizophrenia, Rgs16 is up-regulated in Brodmann Area 10, potentially leading to enhanced inactivation of G-protein signalling [7].

In conclusion, Rgs16 is a crucial regulator in multiple biological processes and disease conditions. Studies using gene-knockout models, especially in cancer, ulcerative colitis, and liver injury, have revealed its role in promoting disease-related cellular processes. Understanding Rgs16 can provide insights into disease mechanisms and potential therapeutic targets.