To achieve selective “role reversal” of TIGIT and combine effective ablation of the CD155-TIGIT axis while promoting NK cell metabolic activity in GBM, we describe a synNotch21-based construct that responds to CD155 as a priming antigen to induce transcriptional activation that results in release of an antibody to block immunometabolic activity in GBM, in this case via adenosine-producing CD73. This evidence concerns the gene TIGIT and glioblastoma.