Extrapolating from reports of pancreatitis attributed to ICIs, one theorized mechanism is CRS, where the robust polyclonal activation of T-cells by blinatumomab leads to an excessive release of cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ), provoking a systemic inflammatory response, causing direct injury to pancreatic tissue, possible reduction in blood flow, and local tissue hypoxia [10]. This evidence concerns the gene TNF and congenital rubella syndrome.