By using astrocytes as the cell of origin in a mouse model of glioblastoma, the loss of p53 function was found to result in significantly increased in growth in vitro and tumorigenesis in vivo of male astrocytes (18); when RB1 and p53 function are used up, both male and female astrocytes put up analogical tumor-forming potential. This evidence concerns the gene TP53 and glioblastoma.