A study using a zebrafish model of MDS with a knockout of RPS14 (uS11), also illustrated in Table 2, sought to find molecules that could improve the MDS phenotype, leading to the discovery of imiquimod, a TLR7 and TLR8 agonist, whose action alleviates anemia by stimulating the expansion of hematopoietic progenitor cells and promoting erythroid differentiation, leading RPS14 mutant MDS patients to a remarkable recovery in the anemia phenotype, due to a modulation of the inflammatory response, when compared to the control group [30]. The gene discussed is TLR8; the disease is myelodysplastic syndrome.