ALK and neuroblastoma: To address whether the ability of oncogenic human ALK to drive the reduced pupal size phenotype is conserved, we employed the pan-neuronal C155-Gal4 driver to overexpress either (1) wild-type human ALK, (2) a human ALK-F1174L gain-of-function mutant (representing an ALK hotspot mutation in neuroblastoma) or (3) an additional ALK-Y1278S gain-of-function neuroblastoma mutant (Umapathy et al., 2019; Vasseur et al., 2019).