In addition to the well-documented involvement of Dyrk1A in neurodegenerative diseases, research has shown that both Dyrk1A and its close relative Dyrk1B are overexpressed in a range of cancers, including glioblastoma, ovarian, lung, colorectal, and pancreatic cancers, suggesting a role in tumorigenesis [12,13,14] According to a study by Pozo et al., Dyrk1A inhibition increased EGFR degradation and inhibited glioblastoma growth via reducing EGFR-dependent tumor growth [12]. Here, EGFR is linked to neoplasm.