The emergence of LLPS provides a novel approach to target intractable and undruggable proteins, for example, it was recently reported that LLPS of disease-associated SHP2 mutants could be specifically attenuated by SHP2 allosteric inhibitors.148 Moreover, LLPS of cancer-associated SRC-1, a previously known transcriptional coactivator for nuclear hormone receptors, could be selectively disrupted by the treatment of an anti-HIV drug elvitegravir (EVG).162 More specific drugs that inhibit the formation of such aberrant condensates are potential new therapeutic cancer treatments. This evidence concerns the gene NR0B1 and cancer.