Interestingly, by means of complementary biophysical techniques, studies have linked the aggregation propensity of distinct regions of the improperly folded C-terminal domain to leukaemogenesis in NPM1-mutated AML; by comparing the conformational and aggregate-forming ability of the entire C-terminal domains of NPM1wt and NPM1c+ the authors reported that only the C-terminus on NPM1c+ and not NPM1wt can form amyloid-like aggregate assemblies (Di Natale et al., 2020; Scognamiglio et al., 2016). The gene discussed is NPM1; the disease is acute myeloid leukemia.