Triple-negative breast cancer (TNBC) is a heterogeneous group of tumors that are defined by the absence of ER, PR, and lack of overexpression of HER2 gene. In this study, we aim to find new targets with therapeutic potential and prove their value through experiments. To screen promising novel therapeutic targets for TNBC, we used RNA-seq profiles of 115 TNBC patients from the TCGA database to construct 115 distinct genome-scale metabolic models and then identified 214 genes that trigger cell death during knockout simulation. Excluding common essential targets, we elicited 18 TNBC-specific gene candidates. Next, we utilized CRISPR KO experimental results of 21 TNBC cell lines in the Depmap database to determine the ability of these 18 genes to induce cell death. Our comprehensive literature review guided us to focus our investigation on the role of the gene KXX in TNBC. Our findings revealed that KXX expression levels were higher in TNBC patients than in healthy individuals, and TNBC patients with the elevated KXX levels had a lower recurrence free survival rate. Furthermore, experimental interventions involving KXX inhibitor or KXX knockdown in TNBC cell lines demonstrated a notable inhibition in the growth of TNBC cells. In vivo, the KXX knock-down tumors grew much more slowly than the tumors in the control group. During this process, we observed the occurrence of apoptosis and ferroptosis, shedding light on the potential mechanisms underlying KXX\'s impact on TNBC.