BRAF and neoplasm: In the case of the most successful anti-oncogene therapies—such as inhibitors of the proteasome machinery, v-raf murine sarcoma viral oncogene homolog B (BRAF) or phosphoinositide 3 (PI3) kinase networks, or cell membrane receptors—the success is partial, as the therapies are highly specific to neoplasia types and are prone to compensatory resistance mechanisms (see the oncogene-specific paragraphs for details and citations).