We hypothesize that the germline absence of normal active p53 (TP53 codes p53 protein) induces alterations of other driver genes that, combined with Inherited Driver Modifier Gene products (IDMGs), generate Dynamic Driver Modifiers Protein-Protein Carcinogenic Networks (DMCN). These DMCNs dictate tumor development type and aggressiveness by altering tumor hallmarks such as proliferation, motility, and cell/tumor morphology. Our overall aim is to identify new signatures and targets for personalized LFS1 treatment and preventive medicine, thus facilitating the treatment and prevention of LFS.