Platelets, traditionally known for their role in hemostasis, are now recognized as key modulators of oncological processes, influencing tumor growth and metastasis through interactions with the tumor microenvironment. Recent studies reveal that platelet activation contributes to T-cell exhaustion by releasing thromboxane A2 (TXA2), which binds to the TBXA2R receptor and activates ARHGEF1, a guanine nucleotide exchange factor (GEF), leading to the suppression of T-cell function. This editorial explores the potential of repurposing anti-platelet drugs, such as aspirin, to counteract these effects. Aspirin, by inhibiting cyclooxygenase enzymes essential for TXA2 synthesis, can enhance T-cell activity in metastatic contexts, thereby improving immune surveillance and response. We advocate for further investigation into the thromboxane pathway’s impact on T-cell functionality and the development of aspirin-based therapeutic strategies to combat cancer metastasis., We advocate for further investigation into the thromboxane pathway’s impact on T-cell functionality and the development of aspirin-based therapeutic strategies to combat cancer metastasis., Finally, this review summarizes gene therapy medicines approved to treat cancer in detail, including names, indications, vectors, and mode of gene therapy. Gene therapy becomes an alternative to an existing management for different diseases..