In line with the above mentioned context, an in vitro study has shown that ceritinib was highly active against tumor clones L1196M, G1269A, C1156Y and I1171T/N/S, which were the top four crizotinib‐resistant mechanisms associated with the acquired ALK mutations.27, 28, 29 Therefore, the early eradication of these tumor clones by the front‐line administration of ceritinib may explain the better therapeutic efficacy, especially a favorable control of systemic progression, than the front‐line use of crizotinib. Here, ALK is linked to neoplasm.