TP53 and ovarian carcinoma: Some examples that sustain this hypothesis include: (i) p53 R248Q mutation, which is highly associated with both breast and ovarian cancers and that decreases p53 DNA binding affinity, increasing the likelihood of p53 to form aggregates (145); (ii) the RGG motif mutation, occurring in FET-family associated proteins, that is associated with pathological protein aggregation (114); (iii) the mutation of TopBP1 in its conserved tryptophan, which is an essential residue for proper ATR activation in a condensate-dependent manner (103, 146).