What is very obvious is that there have been a multitude of genes (74 according to this review) which regulate specifically spina bifida in the mouse. This is a very high number of genes; therefore the take home message would be in our opinion that there are a multitude of genes that can, if perturbed, cause spina bifida. Whether or not these genes cause the condition or are in fact a player in a pool of numerous genes, which can do the job of closing the spinal neural tube, is a tantalising idea. Therefore, we put forth the idea that perhaps these 74 may be working with other genes in their family or other genes which share a common pathway in order to close the neural tube. Furthermore, the idea of gene-gene interaction which promotes heterogeneity among genes is incomplete without also considering the idea of haploinsufficiency of genes, where many mutations in mankind are somehow protected from having a deleterious phenotype by having other genes compensate the job of the gene or genes being perturbed. A very good example of this would be the Vangl-1 and Vangl-2 compound heterozygote mouse mutant which lacks a single allele of both Vangl-1 and Vangl-2; therefore the probability that the 2 genes compensate each other is high and both genes are required in a certain amount of dose, lack of which translates into a neural tube defect phenotype. Therefore, the mouse model which examines the delineation of genes has not completed its true worth until scientists understand the biology of the disease or condition better by also taking into account (i) the amount (the functioning allele) of the said gene and (ii) the interaction with other genes in its family which may be able to compensate its function as well as (iii) the interaction with other genes which share a common pathway. The mouse is a powerful tool to study spina bifida because it is a mammal like humans and its embryology is similar to humans and therefore it is an indispensable tool to mechanistically study the structural changes involved in spinal neural tube closure. The genes involved in spinal neural tube defects may differ in man and mouse; however, parallels may be drawn between the principles of how the genes interact in influencing spinal neural tube closure in both man and mouse.