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In vitro and in vivo analyses suggested that MEK inhibitor-induced PDAC heterogeneity facilitates the rapid proliferation of treatment-resistant cells ( CasRx can precisely and effectively silence the expression of mutant KRAS G12D in PDAC cells and, further, eliminate KRAS G12D -related downstream signaling, thereby, making PDAC cells sensitive to gemcitabine and inhibiting tumor growth ( TABLE 1 Therapies for PDAC directly focused on KRAS mutation or indirectly on related effector

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However, even if they represent a first-line treatment in patients with RA, their use is limited for the development of serious ADRs such as loss of bone mass, increased risk of fractures, infections, diabetes and hypertension [1618]