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Gemcitabine\u2010based chemotherapy regimens have shown limited antitumor effects for PDAC, and combination targets are urgently needed to restrict chemoresistance. We attempted to identify the candidate targets with gemcitabine (Gem) through scRNA\u2010seq and bulk\u2010seq analysis based on chemotherapy\u2010treated and Gem\u2010resistant (GR) samples, respectively. The mechanisms were investigated with experimental validation in vitro and in vivo preclinical PDAC models. We found that chemoresistance and evolution after chemotherapy of PDAC were associated with activation of focal adhesion signal. Mechanistically, the focal adhesion kinase (FAK) inhibitor (IN10018) could restrict chemoresistance to Gem of PDAC by targeting SLC7A11\u2010mediated ferroptosis through PI3K\u2010Akt signaling pathway. 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