AKT1 and neoplasm: In addition to chromatin remodeling, frequent alterations affect the PI3K/AKT/mTOR pathway through inactivation of TSC1 (Tuberous sclerosis complex 1), TSC2 (Tuberous sclerosis complex 2), or PTEN (phosphatase and tensin homolog), resulting in a constitutive activation of mTOR complex 1 (mTORC1) and promoting tumor cell growth, survival, and metabolic reprogramming [19,20,21].