Here, we investigated the functional role of LOXL3 in GBM using CRISPR-Cas9-mediated LOXL3 knockdown in two genetically distinct GBM cell lines: U87MG (wild-type <i>TP53</i>) and U251 (mutant <i>TP53</i>). This evidence concerns the gene TP53 and glioblastoma.