Knl1, also known as CASC5, is an evolutionarily conserved kinetochore-associated scaffold protein. It is essential for accurate chromosome segregation in eukaryotic cells, participating in diverse mitotic processes such as kinetochore assembly, chromosome congression, and mitotic checkpoint signaling [2,4]. These functions are crucial for maintaining genomic stability [3].

Mutations in the Knl1 gene cause autosomal recessive primary microcephaly (MCPH4), highlighting its critical role in brain growth [1]. In cancer research, high expression of Knl1 is associated with poor prognosis in uterine corpus endometrial carcinoma, prostate adenocarcinoma, and colorectal cancer, and knockdown of Knl1 expression can inhibit cancer cell proliferation, invasion, and metastasis [5,6,7]. In cardiomyocytes, regulation of Knl1 by ATF4 (activated by MRPS5 deletion) leads to increased cytokinesis during cardiomyocyte proliferation and improved cardiac regeneration [8].

In conclusion, Knl1 is vital for mitotic processes and genomic stability. Its dysregulation is implicated in diseases like microcephaly and various cancers. Studies, including those using gene-related manipulations in different models, have enhanced our understanding of its role in these biological and disease-related contexts.