This anti-tumor activity was documented with 9-ING-41 monotherapy with enhancement of effect when combined with venetoclax, a Bcl-2 inhibitor, and BAY-1143572, a CDK-9 inhibitor.38 In ATLL, the continual activation and dysregulation of NF-κB through Tax-1 that contributes to tumorigenesis, provides another potential mechanism to explain that clinical activity of 9-ING-41 which warrants further mechanistic studies involving a larger patient cohort.39 The gene discussed is NFKB1; the disease is neoplasm.