AKT1 and neoplasm: Reported mechanisms include: (i) stabilization of HDGF mRNA via IGF2BP3, which enhances glycolysis and angiogenesis [45]; (ii) methylation of ZMYM1, which contributes to the inactivation of the RAS/ERK/c-FOS pathway and reduces E-cadherin expression, thereby facilitating EMT and metastasis [135]; (iii) promotion of ADAMTS9 degradation via YTHDF2, resulting in PI3K/AKT pathway activation and enhanced tumor progression [136].