However, the mutation pathogenicity of variants in one tumor was corroborated by the RNA expression data—tumor 002P had a somatic frameshift mutation in PTEN (a phosphoinositide 3-kinase (PI3K)/AKT/mTOR signaling inhibitor) as well as a non-frameshift deletion and LoH in the FLCN gene (encodes the mTOR complex 2 inhibitor folliculin). Here, AKT1 is linked to neoplasm.