We showed that signaling activation via phosphorylation of SMAD2/3 proteins in response to TGF-β1 is blocked in a heterogeneous manner by dasatinib in different BCP-ALL cell lines, as well as in the dasatinib-resistant RCH-ACV cells, and that inhibition of SMAD2/3 phosphorylation does not correlate with sensitivity to dasatinib [12]. The gene discussed is SMAD2; the disease is acute lymphoblastic leukemia.