Three distinct cancer-associated EML4-ALK variants (V1, V2, V3) can form condensates (Fig. 5B, C, Supplementary Fig. S8A, C), sequester adapters (Fig. 5E–J), and suppress RTK signaling (Fig. 5L, M), regardless of differences in EML4 length, propensity for condensation, and biophysical properties (e.g., solid vs liquid-like)19,20. This evidence concerns the gene EML4 and cancer.