The small molecule QC6352, developed as an inhibitor of the histone demethylase KDM4, exhibits potent anti-cancer activity, and its derivative, zavondemstat, is currently being evaluated in cancer clinical trials. Here, we demonstrate that the anti-proliferative efficacy of QC6352 in glioblastoma models is independent of KDM4 inhibition. Transcriptomic analysis revealed that QC6352's gene expression signature in glioblastoma cells closely resembles that of drugs targeting dihydroorotate dehydrogenase (DHODH). Biochemical assays, protein crystallography, metabolomic analysis, and uridine rescue experiments confirmed that QC6352 inhibits DHODH and thereby disrupts the de novo pyrimidine biosynthesis pathway. This project underscores the ongoing issue of incorrect conclusions caused by the absence of orthogonal high-quality chemical and molecular tools targeting proteins of interest. The mechanism of action of QC6352 is a dual KDM4-DHODH inhibitor and therefore cannot be used to delineate KDM4 function in cells or organisms. We discovered that Zavondemstat, the clinical derivative of QC6352, antiproliferative efficacy is likely due to DHODH inhibition, and has even greater potency than other extensively studied DHODH inhibitors including brequinar and BAY2402234. Thus, this discovery has profound implications on future clinical trials using Zavondemstat