Genetic and functional analysis of the identified fusion genes. (A) Principal component (PC) analysis of gene counts for normal lymph nodes (n = 5), anaplastic large cell lymphoma (n = 5), FTCL (n = 6), and peripheral T-cell lymphoma not otherwise specified (n = 14) using our data and publically available data.^23,24  (B) Partial karyotype illustrating inv(5)(q21q33) masked by t(1;5)(p34;q21) (breakpoints indicated by arrows) identified in patient 1 (upper panel) and metaphase FISH with a dual-color break-apart probe for FER (lower panel). (C) Schematic depiction and DNA sequence trace of the ITK-FER fusion. (D) Complex karyotype, including cryptic t(15;16)(q26;q22), identified by multicolor FISH in patient 2. (E) Metaphase FISH with a dual-color break-apart probe for FES performed in patient 2. (F) Schematic depiction and DNA sequence trace of the RLTPR-FES fusion. (G) Growth curve for Ba/F3 cells transduced with either empty vector or RLTPR-FES. (H) Relative proliferation of Ba/F3 cells transduced with empty vector, SEC31A-ALK, and RLTPR-FES in the presence of increasing concentrations of NVP-TAE684. (I) Western blot assessment of phosphorylated tyrosine residues (band at 131 kDa, corresponding to RLPTR-FES), STAT3 phosphorylation, STAT5 phosphorylation, and AKT phosphorylation in Ba/F3 cells transduced with empty vector or RLTPR-FES exposed to increasing concentrations of NVP-TA684. (J) Heat map representing the expression of STAT3 target genes in CD4⁺ T cells.