These misfolded p53 proteins exhibit a propensity to form aggregates through phase separation.602 Such aggregates not only disrupt the normal function of p53 but also sequester other members of the p53 family, including p63 and p73, thereby further diminishing tumor-suppressive activities and promoting oncogenic processes.603 In cancers where these mutations are prevalent, such as breast and lung cancers, the accumulation of p53 aggregates has been associated with more aggressive disease progression and resistance to conventional therapies.604,605. This evidence concerns the gene TP53 and lung carcinoma.