The exact molecules and the global mechanism that cause AML T-cell impairment may require more investigation, but mechanistic analysis has shown that miR-24-3p acts as an endogenous siRNA for DENN/MADD; moreover, miR-24-3p overexpression by itself affected T-cell viability through the inhibition of the NF-κB, JAK/STAT and ERK signaling pathways, which were reported as an important regulator of both T-cell function and cytokine production. This evidence concerns the gene SOAT1 and acute myeloid leukemia.