For example, a PI3Kδ specific inhibitor (CAL‐101/idelalisib) has shown promising results in the treatment of patients with relapsed/refractory CLL.20, 21 However, the efficacy of PI3K inhibitors, like most targeted drugs, is limited by concurrent activation of other pro‐survival and growth‐related pathways that lead to drug resistance.22 A potential strategy to overcome these limitations is combining PI3K inhibition with drugs that target other pathways, in order to achieve synergistic anti‐tumour activity. The gene discussed is PIK3CD; the disease is neoplasm.