Note, for instance, that heterozygote Marcksl1 deficiency is sufficient to generate a low penetrant, yet severe neural tube defect in mice [36], and a mere two-fold overexpression of MARCKS reduced noradrenaline release from neuroblastoma cells by 50%, possibly by promoting actin crosslinking, thereby restricting the movement of dense-cored vesicles carrying this neurotransmitter [37]. This evidence concerns the gene MARCKSL1 and neuroblastoma.