Overexpression of NetB^{Scer\UAS.T:Hsap\MYC}, under the control of Scer\GAL4^MH56, which has strong activity in the lamina neurons L3 throughout pupal development, does not interfere with R8 axon targeting.

Expression of NetB^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^MH56 in a Df(1)NetAB^Δ background significantly rescues the R8 axon-targeting defects. Only 8% of Rh6-expressing neurons stall at the medulla neuropil border or terminate in the distal M1/M2 layers, compared to 61% in mutant siblings lacking NetB^{Scer\UAS.T:Hsap\MYC}.

Ectopic expression of NetB^{Scer\UAS.T:Hsap\MYC} throughout the somatic and visceral mesoderm, driven by Scer\GAL4^twi.PB, causes salivary gland guidance defects. In 16% of these embryos, the distal tip of the salivary gland splits into two branches; one branch continues to migrate along the visceral mesoderm, while the other migrates towards lateral somatic muscles. Expression of NetB^{Scer\UAS.T:Hsap\MYC} throughout the CNS, driven by Scer\GAL4^sca.PU, causes the distal tip of the salivary gland to become curved medially toward the CNS, instead of lying parallel to the CNS. However, expression of NetB^{Scer\UAS.T:Hsap\MYC} in the CNS with Scer\GAL4^elav.PLu, does not cause misorientation of the salivary gland.

When expression is driven by Scer\GAL4^how-24B SNa axons often stall at the edge of the CNS or fasciculate with the ISN.

Scer\GAL4^sca-537.4 and Scer\GAL4^elav.PLu induced expression in embryos causes commissures that are thinner or nearly absent and bundles of axons that project inappropriately laterally toward the edge of the CNS leaving gaps in the longitudinal tracts. Scer\GAL4^how-24B induced expression causes excessive branching of the intersegmental nerve and these branches to stall short of their targets.