KRAS and neoplasm: Inhibiting the formation, release, or uptake of EVs is anticipated to be a pivotal strategy for blocking the progression of KRAS‐mutant PDAC.[5] Among these, EVs harboring oncogenic KRASG12D‐specific short interfering RNAs (siRNAs) demonstrated sustained tumor‐suppressive effects in an orthotopic xenograft model of PDAC, addressing the challenge of targeting KRAS mutations.[5a] Thus, EVs may be crucial regulatory mediators of metastasis, including PNI, in KRAS‐mutant PDAC.