Inhibiting TLR2 or Akt/mTOR signaling mitigated MDSC differentiation, suggesting a potential therapeutic strategy to counter MDSC‐mediated immune suppression in AML, highlighting the significance of EV‐associated palmitoylated proteins in disrupting leukemogenesis and improving immune responses, thereby enhancing antitumor immune responses and improving patient outcomes in acute myeloid leukemia [38], as illustrated in Table 1. The gene discussed is TLR2; the disease is acute myeloid leukemia.