In agreement with these findings, a previous study reported that miR-29b was downregulated in CML and overexpression of miR-29b in K562 cells inhibited leukemic cell growth and promoted apoptosis through regulation of the BCR-ABL1 tyrosine kinase (Li et al., 2013). The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.