Moving forward, we propose a dual-axis therapeutic model: (1) development of tumor-selective delivery systems, such as ligand-directed nanoparticles or TME-responsive prodrugs, to confine ADAR1 inhibition to malignant tissues; and (2) implementation of isoform-specific RNA-based modulators, such as splice-switching oligonucleotides, to selectively target ADAR1-p150 without affecting p110. Here, ADAR is linked to neoplasm.