Demireva and colleagues also found similar motor pools mispositioning phenotype can be attributed to the inactivation of N-cadherin, which strongly suggests a prominent requirement of both ?-catenin and ?-catenin in the cadherin/catenin signalling pathway. These findings correspond to the report that ?-catenin recruited to N-cadherin is essential for the contraction of smooth muscle and this protein-protein interaction is mediated by actin polymerization (Wang et al., 2015). Conspicuously, this cooperative function of ?-catenin and ?-catenin offers a potential explanation of the condition when a stronger influence on neuronal differentiation is produced by N-cadherin mutants over ?-catenin mutants alone (Kadowaki et al., 2007). However, combined with the previous study by Price et al., 2002 which implied that both N-cadherin and type II cadherins regulate motor neuron settling, another concern would be the possibility of protein compensation during this genetic manipulation. One could argue that the disruption of cadherin/catenin might result in compensational effects caused by the activation of other cell-cell interaction pathways such as Notch signalling pathway, which is also believed to play important roles in spinal cord development and regeneration (Losada et al., 2017). Moreover, notwithstanding a universally accepted fact that motor pool formation is only affected by cadherins (Luxey et al., 2015), it could be that type II cadherins are facilitating N-cadherin to achieve motor pool coalescence (Bello et al., 2012). Accordingly, the function of cadherins in motor neuron assembling remains oblique considering the diversity of cadherin family (Demireva et al., 2011; SDasen, 2017)Nevertheless, this discovery produces widespread implications in genetic manipulation of motor neuron topography. Given that cadherin/catenin signalling is a core event of cell adhesion in neuronal body assembling, researchers could infer that developmental processes which highly rely on cell adhesions like migration and nucleogenesis are also based on somatic positioning (Montage et al., 2017). Another intriguing question this finding has led to is whether cadherin/catenin signalling can alter the formation of neuromuscular junction. This was somehow answered since the overexpression of ?-catenin in muscles was found to produce an abnormal distribution of receptors on the pre- and post-synapse during neuromuscular junction development (Wu et al., 2012). Notably, the conditional elimination of catenins in chicken showed a much worse phenotype in terms of lateral migration, suggesting that the impact of cadherin/catenin manipulations could vary in different species due to different gene expression profiles (Bello et al., 2012). In addition to the biological conclusion, the fluorophore-conjugated secondary antibodies and retrograde labelling used in Demireva’s study has been applied in other research to tag spinal cord neurons, besides, the columnar mixing index (Cmi) developed in this study allows a general calculation of the neuronal mixing level between different columns (Mendelsohn et al., 2017; Hanley et al., 2017).