AKT1 and neoplasm: Canonical ALK fusion proteins, such as EML4-ALK, undergo dimerization mediated by the N-terminal fusion partner, stabilizing the C-terminal tyrosine kinase domain and persistently activating downstream signaling axes, including RAS-MAPK, PI3K-AKT, and JAK-STAT, thereby promoting tumor cell proliferation, survival, and migration [25].