Clinical highlights. (A) Novel fusions involving druggable targets such as ALK, BRAF, FLT3, JAK2, and ROS1 (5′ partner salmon, 3′ partner including kinase domain of target gene gray; ALCL, anaplastic large cell lymphoma). (B) Distribution of IGH rearrangement partners. (C) Overexpression of (i) FGFR3 and (ii) WHSC1 in t(4;14)-positive MM cases (n = 61) compared with t(4;14)-negative MM cases (n = 388). The violin plot shows the distribution of the log expression ratios of FGFR3 and WHSC1 in each group, respectively. For both cases, the difference is statistically significant (FGFR3, P = 8.7e⁻²²; WHSC1, P = 5.28e⁻³², 1-sided Wilcoxon rank-sum test). (Ciii) Overexpression of CCND1 in all t(11;14)-positive cases (n = 67) compared with t(11;14)-negative cases (n = 3095). The difference is also statistically significant (P = 6.00e⁻³⁸, 1-sided Wilcoxon rank-sum test). (D) Overview of short variants (single nucleotide variants [SNVs], ITDs, indels) and large-scale aberrations including long deletions, copy number gains, and fusions detected in FLT3. The FLT3 protein is drawn with its immunoglobulin-like (Ig, red), transmembrane (Tm, steel blue), and tyrosine kinase (Tk, peach) domains illustrated. Positions and protein effect of all short variants are indicated. For ITDs (green), samples with ITD at the same positions are aggregated together regardless of the actual insert sequence. The ranges of large-scale aberrations are indicated with light blue bars. Commonly tested “hotspot” mutations are shaded in gray.