While our findings demonstrate that combining BCL-XL inhibitors with BRAF inhibitors robustly induces apoptosis in BRAFV600E CRC cells in vitro, the clinical use of BCX-XL inhibitors is currently limited by their induction of thrombocytopenia [30], an on-target toxicity driven by the high dependency of platelets on BCL-XL for their survival [31]. The gene discussed is BCL2L1; the disease is Thrombocytopenia.