S2 Fig illustrates that helical substate distributions largely stabilize by the end of 200-ns RE-GA simulations for both the wild-type p53-TAD and its cancer mutants and that the final distributions from the control and folding runs are largely consistent. Furthermore, as shown in Fig 3, the structural ensembles derived from the control and folding simulations of the wild-type protein contain essentially identical sets of long-range contacts and with largely similar probabilities. This evidence concerns the gene TP53 and cancer.