To do this we activated human ALK (Fig. 4A) in three ways by ectopically expressing: (1) human ALK with the ALKAL1 ligand, which leads to high levels of ALK signaling activity4 (Fig. 4A,C), (2) a constitutively active ALK variant (ALK-F1174L) commonly observed in neuroblastoma patients12–16 (Fig. 4A,D), and (3) the chimeric NPM1::ALK oncogene found in anaplastic large cell lymphoma8 (Fig. 4A,E). The gene discussed is ALK; the disease is neuroblastoma.