The ongoing development of STING agonists for cancer treatment prompted a comprehensive analysis of the ability of eribulin to enhance the activity of cyclic di-nucleotide STING agonists (e.g., cGAMP, ADU-S100, E7766), as well as small molecule non-cyclic di-nucleotide STING agonists (e.g., MSA-2) (Figure 1B) [32]. The gene discussed is STING1; the disease is cancer.