The initial study on a VIM–KMT2A sarcoma demonstrated high expression of KMT2A and the downstream target HOXA genes [3], likely driven by the highly active VIM promoter in the VIM–KMT2A fusion, with retention of both CxxC-binding and RD2 domains in KMT2A that allow PAFc-associated chromatin modification of HOX-related genes. The gene discussed is PRPH2; the disease is sarcoma.