Interestingly, SEMA3C has been previously demonstrated to be fundamental for NC development (Schulz et al., 2014b), and a recent tumor transcriptional profiling showed that NBM invasiveness is induced by the shutdown of SEMA3C, which functions as a pro-cohesion autocrine signal to constrain the tumoral mass (Delloye-Bourgeois et al., 2017). The gene discussed is SEMA3C; the disease is neoplasm.