In cancer treatment, prodrugs like PRIMA-1 and its derivative PRIMA-1MET present a viable method for attacking "undruggable" targets such mutant p53. These molecules restore the active conformation of mutant p53, therefore producing sequence-specific DNA binding and cellular death. With their active metabolite methylene quinuclidine alkylating p53 and re-establishing an oxidative environment inside tumour cells, PRIMA-1 and PRIMA-1MET, most importantly, behave as prodrugs. Small compounds such as nutlins also help to solve the "undruggable" target problem by blocking the interaction between p53 and MDM2, a negative regulating protein that drives p53 breakdown. Nutlins offer great potential in preclinical and clinical contexts and help to stabilise p53, therefore keeping its tumour-suppressing properties. These creative approaches draw attention to the possibilities for efficiently modifying difficult cancer targets by the use of prodrugs and tailored compounds ([132]).