As the field progresses, advanced trispecific TCE combining tumor targeting, T-cell engagement (anti-CD3), and co-stimulation (anti-CD28) or checkpoint inhibition (anti-PD-1) could be further potentiated by co-administering therapies that upregulate local CXCL10, transforming recruitment from a passive to an active process and overcoming a major barrier in solid tumor immunotherapy [163,188]. This evidence concerns the gene CXCL10 and neoplasm.