In this context, DYRK1B overexpression may help maintain a reversible quiescent state or inhibit cancer cell proliferation [116,117,118], while DYRK1B reduction can drive cell cycle entry in quiescence (by reducing the DYRK1B expression in PDAC or by DYRK1B inhibition in CRC cell lines) [119]. Here, DYRK1B is linked to cancer.