Gliomas are a family of primary central nervous system tumors of variable malignancy that are derived from supporting glia (astrocytes, oligodendrocytes, ependymal cells) or their progenitors/stem cells. There are two potential strategies to prevention: preventing gliomas from forming and preventing lower-grade gliomas from developing into higher-grade gliomas. Each would lower time-dependent mortality. Each also depends on an understanding of what causes gliomas so that these factors can be modulated. In this presentation, I will discuss primary prevention, chemoprevention, and screening. I will first focus on the known chromosomal, genetic, and protein changes associated with the different histologic varieties of glioma and the environmental, hereditary, and infectious/viral factors that may promote glioma development and malignant progression. I will discuss a number of clinical scenarios that eventuate from the known genetic patterns of these tumors and the changes in genetic patterns that reflect malignant progression. The basic thinking is that if one could prevent specific gene mutations and/or deletions or gains of specific chromosomes that lead to the development of low-grade (WHO 2) gliomas, then theoretically this would reduce the occurrence of high-grade (WHO 3 and 4) gliomas and hence the almost certain death that now is the fate of most patients with these tumors. In the case of de novo WHO 3 and 4 tumors, being able to prevent or counter specific gene mutations and/or the deletion of specific chromosomes would in itself reduce the occurrence of these gliomas and increase survival. Alternatively, a curative treatment for low-grade glioma that prevents these chromosomal/gene changes would prevent some glioblastomas (WHO 4) from forming and would have the same desired effect on survival. Obviously, for the latter to be achieved, we must also be able to diagnose and treat low-grade gliomas earlier.