In line with this concept, the phenotypic clustering of drugs depended on the sample selection; when we performed the same analysis on the T cell prolymphocytic leukemia (T-PLL) samples, the cluster of BCR-targeting drugs largely dissolved, while other clusters (reactive oxygen species [ROS], Bcl-2 homology domain 3, BH3 mimetics) — less dependent on disease-specific activity — remained (Supplemental Figure 6). Here, BCR is linked to prolymphocytic leukemia.