Given that other components of innate immune signaling including MyD88, MAVS, RIG-I, and TLR4 can undergo alternative splicing in response to infection (22), it is intriguing to speculate that oncogenic signaling or cancer-related inflammation can initiate alternative splicing in STING and could be a generalizable phenomenon beyond the context of AML. This evidence concerns the gene TLR4 and acute myeloid leukemia.