Initially pinpointed as a selective inhibitor of dual-specificity tyrosine phosphorylation-regulated kinase 1a (DYRK1A) in glioma cells [71, 79], harmine's therapeutic efficacy is compromised by its off-target inhibitory effect on monoamine oxidase-A (MAO-A), inducing degradation and reuptake of monoamines such as serotonin and norepinephrine, consequently impacting various targets within the nervous system [80, 81]. Here, MAOA is linked to glioma.