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English: Figure 1. ALK-rearrangement-targeted cancer therapy in non-small cell lung cancer. EML4-ALK translocation activates PI3K-AKT, RAS, and JAK/STAT signaling cascades, thereby influencing tumor progression, survival, and growth. ALK inhibitors such as crizotinib, alectinib, and brigatinib act on mutated ALKs, such as ELM4-ALK, and suppress the production of ALK fusion protein resulting from ALK rearrangement. EML4-ALK, echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase; ALK, anaplastic lymphoma kinase; PI3K, phosphatidylinositol-3 kinase; mTOR, mammalian target of rapamycin; RAS, reticular activating system; MEK, mitogen-activated extracellular signal regulated kinase; ERK, extracellular signal-regulated kinase (ERK); JAK, Janus kinase; STAT, signal transducer and activator of transcription.