**Core Concept**
FLT-3 (Fms-like tyrosine kinase 3) mutations, particularly internal tandem duplications (ITDs) and point mutations in the tyrosine kinase domain, are common in acute myeloid leukemia (AML). These mutations lead to constitutive activation of the FLT-3 receptor, promoting cell proliferation and survival. Targeted therapies aim to inhibit this aberrant signaling.

**Why the Correct Answer is Right**
The treatment of choice for AML with FLT-3 mutations involves the use of FLT-3 tyrosine kinase inhibitors (TKIs), which block the phosphorylation of FLT-3, thereby inhibiting its downstream signaling pathways. This leads to reduced cell proliferation and increased apoptosis of leukemic cells. The most commonly used FLT-3 TKI is midostaurin, which has been shown to improve overall survival in patients with FLT-3 mutated AML.

**Why Each Wrong Option is Incorrect**
**Option A:** This option is incorrect as it does not specify a targeted therapy for FLT-3 mutated AML. Chemotherapy and other conventional treatments may not be as effective in this subset of patients.
**Option B:** This option is incorrect as it does not address the specific mutation in FLT-3. Other tyrosine kinase inhibitors may not be as effective against FLT-3 mutated AML.
**Option C:** This option is incorrect as it does not accurately represent a treatment for FLT-3 mutated AML. Other targeted therapies may be more effective in this subset of patients.

**Clinical Pearl / High-Yield Fact**
It's essential to recognize the importance of genetic mutations in guiding treatment decisions in AML. Patients with FLT-3 mutated AML may benefit from targeted therapies, which can improve outcomes and reduce the risk of relapse.

**Correct Answer:** C. Midostaurin.