In this context, our work indicates that AAMDC could just be such a biomarker and that targeting AAMDC signaling with PI3K-AKT-mTOR inhibitors and potentially more specifically, targeting key binding interfaces with effectors (such as the PTB domain of RabGAP1L), may be an effective and more selective treatment for IntClust2 cancers or other malignancies that have AAMDC amplification. The gene discussed is MTOR; the disease is cancer.