Secreted effector that, with CRN115, is critical to pathogenesis by modulating host defenses (PubMed:21071601). Induces cell death in plant host cells (PubMed:21071601). Suppresses callose deposition and affects expression of defense-related genes including two salicylic acid (SA) signal-induced and antimicrobial PR genes (PR1 and PR2), and genes involved in jasmonic acid (JA)/ethylene (ET)-mediated defense pathway (ERF1, ORA59, PDF1.2) (PubMed:27243217). CRN115 and CRN63 may share the same molecular host targets that are involved in the cell death signal transduction pathway and that their differential activities are dependent on plant nuclear localization or not (PubMed:21071601). Does not affect MAPK activation and BIK1 phosphorylation and acts downstream of the MAPK cascades in PTI signaling (PubMed:27243217). Forms a homodimer via an inverted association manner (PubMed:27243217). Forms heterodimers with CRN79 and CRN115 (PubMed:27243217). Expression is constitutively high and slightly induced during the late infection stages (approximately 1.5-fold). The CRN proteins have modular architectures that include a signal peptide, a conserved N-terminus, and highly diverse C-terminal domains. The conserved CRN N-terminus harbors a distinct LXLFLAK motif, which is followed by the conserved DWL domain. A highly conserved HVLVXXP motif marks the end of the CRN N-terminal domains and forms a junction where diverse C-terminal domains are fused. The conserved CRN N-terminus mediates the translocation into the plant host cells. The C-terminal effector region is sufficient for its activity within the host cell. The predicted NLS is required for its function to induces cell death in plant host cells. Leads to a reduction of virulence on soybean. Belongs to the Crinkler effector family.