The activation of PAR1 involves the release of an N-terminal peptide and the exposure of an otherwise hindered ligand, resulting in an exclusive mode of activation and a general paradigm for the entire PAR family (1–3). While a well-known classical observation points to a tight link between hyper-activation of the coagulation system and cancer malignancies, the molecular mechanism that governs pro-coagulant tumor progression remains poorly defined [1], [2], [3]. Here, MARK2 is linked to neoplasm.