Individual mutations prove particularly detrimental under conditions of enforced DNA stress, such that classical cytostatic drug treatments or reduction therapies (involving paclitaxel, doxorubicin, or γ-irradiation) may paradoxically impose adverse effects, as can be deduced, e.g., from p53 mutant-dependent responses to neoadjuvant therapy in breast cancer [141,142]. Here, TP53 is linked to breast cancer.