Because multiple studies have shown that the survival advantage of certain cancers depends on the activity of overexpressed aurora kinases and polo‐like kinases (PLK) [47, 48] and both kinases co‐regulate many cellular processes governing cell division by activating specific cyclin‐dependent kinases (CDKs) and their associated cyclins, we examined the expression of PLK1 protein in naïve, short‐term tozasertib‐treated, and tozasertib‐resistant adult and pediatric glioma cell lines. The gene discussed is PLK1; the disease is cancer.