Ktn1, known as kinectin 1, is associated with various biological processes and diseases. It has been implicated in pathways such as cell cycle, DNA replication, and microRNAs in cancer [1]. In normal physiological processes, it may play a role in cell survival, migration, and invasion, as well as in the regulation of cell cycle and apoptosis. Genetic models can be valuable for studying its function.

In hepatocellular carcinoma (HCC), Ktn1 expression is increased, and high expression is correlated with poorer prognosis. Knockout of Ktn1 in Huh7 cells inhibited the viability, migration, and invasion ability of HCC cells, increased the proportion of cells in the G0-G1 phases, and elevated apoptosis rates [1]. In attention deficit hyperactivity disorder (ADHD), Ktn1 variants were significantly associated with the disorder, and the major alleles of risk variants increased putamen volumes [2]. In Parkinson's disease (PD), certain Ktn1 variants increased the risk for PD and putamen gray matter volumes, and also increased Ktn1 mRNA expression in the putamen or substantia nigra pars compacta [3].

In conclusion, Ktn1 plays important roles in cell survival, migration, invasion, cell cycle, and apoptosis as revealed through functional studies. Gene knockout models in HCC, ADHD, and PD have helped uncover its contributions to these disease areas, indicating its potential as a therapeutic target in HCC, and highlighting its role in the development of ADHD and PD.