DYRK4, a member of the dual-specificity tyrosine phosphorylation-regulated kinase family, plays important roles in multiple biological processes. It is involved in antiviral innate immunity, cell differentiation, proliferation, and survival. It has been associated with pathways related to interferon-β induction and may have a role in spermatogenesis as well [1,4,5]. Genetic models, such as knockout mice, can be valuable tools for studying its functions.

In antiviral innate immunity, DYRK4 acts as a scaffold protein. Overexpression of DYRK4 enhances virus-triggered activation of IRF3 and type I IFN induction, while knockdown or knockout of DYRK4 impairs virus-induced activation of IRF3 and NF-κB. Dyrk4-knockout mice are more susceptible to viral infection, suggesting its importance in antiviral defense [1]. In the context of cancer, hypomethylation of DYRK4 in peripheral blood is associated with an increased lung cancer risk. Also, a novel neoplastic fusion transcript, RAD51AP1-DYRK4, is preferentially expressed in luminal B breast tumors, endowing increased sensitivity to the MEK inhibitor trametinib [2,3].

In conclusion, DYRK4 is crucial for antiviral innate immunity and is associated with cancer-related processes. The use of Dyrk4-knockout mouse models has provided insights into its role in antiviral responses and potential implications in cancer. Understanding DYRK4 functions can contribute to developing strategies for treating viral infections and certain cancers.