EGFR and non-small cell lung carcinoma: As for target mutations, different genetic alterations associated with resistance have been described for ALK-positive NSCLC: i) L1169M within the “gatekeeper” domain (the most frequent); ii) L1152R, associated with EGFR signaling activation; iii) G1202R and S1206Y within the ATP-binding pocket, leading to a decreased Crizotinib affinity [116].