Studies in cell culture and knock-in mouse models have yielded a thorough mechanistic understanding of the functional impact of hotspot mutations, which have largely lost the tumor suppressive activity of the wild-type proteins (LOF, loss-of-function) and, by oligomerization, exert additional dominant-negative activity towards wild-type p53 expressed from a remaining non-mutated allele [5]. Here, TP53 is linked to neoplasm.