The discovery of a signalling pathway that promotes the survival of cancer-initiating cells in chronic myeloid leukaemia (CML) could aid the design of new treatment regimes. The find is reported in this week’s Nature.

Leukaemia-initiating cells (LICs) are the small, slowly dividing subset of cells that drive the recurrence of certain types of leukaemia. Atsushi Hirao and colleagues show that the TGF-–FOXO signalling pathway has an essential role in the maintenance of these cells, and that treatment with a TGF- inhibitor impairs the ability of cultured LICs to cause cancer growth.

CML occurs when specific regions of two particular chromosomes swap over, yielding a cancer-causing tyrosine kinase that is permanently ‘switched on’. But although the tyrosine-kinase-blocking drug imatinib kills leukaemia cells, it fails to target LICs, meaning that remission can sometimes be short-lived. Combining imatinib with a TGF- inhibitor could be a potential answer, the authors speculate, as the strategy appears promising in a mouse model of CML.