Recent genomic and immunobiology work has sharpened our understanding of SPTCL; germline loss‐of‐function variants in HAVCR2 (TIM‐3) are seen in a meaningful subset, especially in patients with HLH, linking defective TIM‐3 signaling to unchecked immune activation [24, 25]. This evidence concerns the gene HAVCR2 and hemophagocytic syndrome.