p53 is a critical tumor suppressor gene and is mutated in more than 50% cancers. p53 is part of a larger family of genes known as the p53 family, which includes p63 and p73. The functional roles of p63 and p73 in cancer is complex due to the existence of multiple isoforms and the lack of antibodies that distinguish between them. The isoforms can be placed into two groups: the TA isoforms, which structurally resemble p53 and act as tumor suppressors, and the ΔN isoforms, which bind to p53, TAp63, and TAp73 and inhibit their function, thus acting as oncogenes. Many current therapies for cancer patients and molecular studies target p53 only, ignoring the existence of the other p53 family members. p53 reactivation suppresses tumors in-vivo, yet this strategy has proven difficult to implement therapeutically. One alternative strategy to overcome p53 loss is to manipulate the p53 family members, p63 and p73, which interact with p53. We hypothesize that through manipulation of the p53 family we can shrink tumors that are deficient or mutant for p53.