ASCENDing the anaplastic lymphoma kinase ladder: a tale of two C-nibs

Targeting driver mutations in oncogene addicted advanced non-small cell lung cancer (NSCLC) has revealed the Achilles heel and revolutionized its management in the last one decade (1). At present, approximately 2/3^rd of lung adenocarcinomas can be classified based on the driver genomic alteration (2). Anaplastic lymphoma kinase (ALK) gene rearrangement, particularly EML4-ALK fusion is seen in 3−7% patients of NSCLC, more so in younger patients and non-smokers (3-5).