This is supported by the cytokine profile upon FAP inhibition highlighting the role of FAP in tumor cell behavior and TME, which is enhanced by the activation of the MAPK pathway via the TGF - PARP1/2 - PLCβ axis, known to be regulated by the phosphorylation of PLCs via G coupled protein activation [36] accompanied by higher uPA, VEGF and IL8 levels [37, 38]. Here, PARP1 is linked to neoplasm.