"Rose Bengal has been studied recently in several malignancies as an intralesional therapeutic agent. Experiments evaluating the mechanism of action demonstrate that RB is taken up selectively in the lysozomes of transformed cells [8,9,16]. It induces cell death by apoptosis and necrosis. Upon treatment with RB in-vivo, many treated patients and animals have been found to generate a systemic anti-tumor response resulting in growth suppression of untreated lesions. RB-mediated tumor cell death may expose tumor antigens that may otherwise evade immune detection. Upon re-exposure to these antigens, a robust cytotoxic T-cell response has been demonstrated in experimental models. Though most profoundly described in melanoma cells, clearly an immunoreactive malignancy, the effect has been shown to be not limited to one specific type of malignancy. Our current research is establishing the role of RB in generating anti-tumor immune responses in gastrointestinal cancer and liver metastases. Decrease in tumor burden and stimulation of an immune response with PV-10 has been demonstrated in animal models of metastasis, and correlations of these responses in clinical studies is consistent with such results. That PV-10 treatment can potentially increase circulating cytotoxic T-cells, even in patients who were previously treated with immune-activating checkpoint blockade, supports the possibility that RB induced cytotoxicity may activate T-cells that are responsible for the bystander effect on untreated lesions [19,21]. As such, intralesional therapy with RB may be a promising new mode of therapy to stimulate T-cell mediated anti-tumor immune responses."