On the other hand, “αC-OUT” inhibitors, such as vemurafenib and dabrafenib, have important clinical implications and have been observed to induce less paradoxical activation, likely due to decreased RAF/MEK interaction in this conformation.29,30,33,48 Although paradoxical activation limits the use of type I BRAFi in cancer therapy, their role is beneficial in scenarios where this activation is desired, such as wound healing,49 promoting podocytes survival,50 and here, erythropoiesis. The gene discussed is RAF1; the disease is cancer.