“…The EML4-ALK fusion has been detected in 3.7% to 7% of NSCLCs (10, 14), usually in adenocarcinomas with signet-ring cells or cribriform histology features, and is more common in young patients who have never smoked (14). There are several EML4-ALK rearrangement variants and also ALK fusion with other less frequent partners, such as kinesin family member 5B ( KIF5B ), TRK-fused gene ( TFG ), kinesin light chain 1 ( KLC1 ), and huntingtin-interacting protein 1 ( HIP1 ) genes, resulting in oncogenic transformation (13, 15). It has been shown that EGFR , Kirsten rat sarcoma viral oncogene homolog gene ( KRAS ), and ALK molecular alterations are mutually exclusive events (4); nevertheless, they have been described in up to 2.7% of lung adenocarcinoma cases with concurrent molecular alterations (16).…”