Collectively, co-culturing with HS-5 cells resulted in the aberrant activation of Hh pathway and subsequent BCR-ABL overexpression in K562 cells which could contribute to IM resistance of CML, whereas OAG sensitized K562 cells to IM treatment through inhibiting Hh pathway and then BCR-ABL expression in vitro and in vivo. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.