This notion is supported by a recent study that inhibition of TGF‐β signaling enhanced rather than suppressed the anemia in sf3b1 mutants.[49] Thus, these findings indicate that the TGF‐β/Smad2 signaling pathway is much more complex than previous thought, and it will be of interest to explore the mechanisms underlying the different roles of TGF‐β/Smad2 signaling in erythropoiesis under both physiological and pathological conditions in future studies. This evidence concerns the gene SMAD2 and anemia (phenotype).