At the level of molecular mechanisms, ZKSCAN3 drives the malignant phenotype through a multi-targeted transcriptional regulatory network: (1) transcriptional activation of MEK2, RasGRP2, IGF-2, and ITGβ4 (key effector molecules) promotes proliferation; (2) activation of the MST1R signaling axis enhances migration; (3) induces VEGF-mediated tumor angiogenesis; and (4) up-regulates matrix metalloproteinase 26 (MMP26), cathepsin D, and protein hydrolases such as serine protease 3 (PRSS3) to enhance invasive potential [76]. The gene discussed is PRSS3; the disease is neoplasm.