Currently, many of the newly developed synthetic STING agonists are able to bind all or most common isoforms of human STING resulting in increased production of type I IFNs leading to enhanced T cell activation,[61] followed by tumor regression[62] in various mouse models such as colorectal cancer[62, 63] or acute myeloid leukemia (AML)[62a] (as summarized in Table1). The gene discussed is STING1; the disease is neoplasm.