In summary, dissection of the mechanisms underpinning combinatorial ALK and PI3Kβ inhibition efficacy suggest that the sensitization of ALK‐rearranged cancer cells to ALK inhibition by selective PI3Kβ inhibition was, at least in part, mediated through a blockade of EGFR‐mediated rebound activation of MAPK and PI3K‐AKT signaling, enhancing cell death (Fig. 6). The gene discussed is ALK; the disease is cancer.