FLC tumors contain a unique genetic defect that fuses together portions of genes called DNAJ and PKAc. DNAJ helps fold other proteins into their correct shapes, whereas PKAc is an enzyme involved in cell communication. An FCF supported research team at the University of Washington, Seattle now report that the DNAJ-PKAc fusion additionally recruits the co-chaperone Hsp70 and enzymes that promote uncontrolled cell growth. Turnham/Smith and colleagues have also discovered combinations of drugs that simultaneously target these enzymes to slow the growth of FLC cells. Future pharmacological studies will test these drug combinations on human FLC cells and in mouse models. Click here to read the published article in e-LIFE.