AKT1是致癌基因，编码一种丝氨酸/苏氨酸蛋白激酶，为PI3K信号传导途径中的关键下游调节因子。 AKT1可激活许多下游底物，包括GSK3，FOXO和mTORC1，它们对细胞存活，增殖和代谢至关重要；当PI3K信号传导被PTEN磷酸酶活性终止时，AKT1发生负调节。 AKT1通常通过激活PI3K途径或通过PTEN的失活在癌症中被激活。在人类癌种中已经鉴定了AKT1的激活突变和罕见的AKT1基因扩增。体细胞AKT突变已经在人类乳腺癌、结直肠癌、卵巢癌中有所报道。在胃癌中，有研究显示AKT发生扩增。AKT信号通路在许多癌症的肿瘤形成和进展中起着重要作用，包括恶性神经胶质瘤。

AKT1 is a serine/threonine protein kinase that is a critical downstream effector in the PI3K (phosphoinositide 3-kinase) signaling pathway. AKT1 can activate a number of downstream substrates, including GSK3, FOXO and mTORC1, which are critical for cellular survival, proliferation, and metabolism. Negative regulation of AKT1 occurs when PI3K signaling is terminated by PTEN phosphatase activity. AKT1 is frequently activated in cancers, typically through activation of the PI3K pathway or by inactivation of PTEN. Activating mutations in AKT1 and infrequent AKT1 gene amplification have been identified in human cancers, which allow for phosphoinositide-independent AKT1 activation. AKT somatic mutations have been reported in human breast cancer, colorectal cancer, and ovarian cancers. AKT amplification has been indentified in gastric adenocarcinoma. The AKT signaling pathway plays an important role in tumor formation and progression in many cancers, including malignant gliomas.

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