Pathological and genetic findings in BIA-ALCL. (A) Distribution of genetic subtypes in systemic, cutaneous, and breast implant–associated ALCL. −/−/−, triple-negative. (B) Low-power hematoxylin and eosin–stained image of a capsulectomy specimen showing the fibrous capsule (*), an inner layer of lymphoma cells (‡), and the original location of the implant and surrounding effusion (¶). Image was taken using an Olympus DP71 camera, Olympus BX51 microscope, and Olympus cellSens image acquisition software (original magnification ×40). (C) High-power hematoxylin and eosin–stained image of the capsule shows a cluster of large pleomorphic cells (original magnification ×1000). (D) Immunohistochemistry for CD30 shows strong and uniform staining in the neoplastic cells (original magnification ×1000). (E) Immunohistochemistry for ALK shows absence of staining in the neoplastic cells (original magnification ×1000). (F) Immunohistochemistry for pSTAT3^Y705 shows strong nuclear staining in the neoplastic cells (original magnification ×1000). (G) Mutations in JAK1 and STAT3 in BIA-ALCL. Pkinase_Tyr, protein tyrosine kinase domain; SH2, Src homology 2 domain; STAT_alpha, all-α domain; STAT_bind, DNA binding domain; STAT_int, protein interaction domain.