We investigated here whether Necl-4 (also termed TSLL2, IGSF4C, SynCAM4, or CADM4) [14–16] also regulated the contact inhibition of cell movement and proliferation, because it binds protein-tyrosine phosphatase, non-receptor type 13 (PTPN13, also termed PTP-BL, PTP-BAS, PTP-L1, or FAP1), a putative tumor suppressor, through the cytoplasmic region of Necl-4, and inhibits the heregulin-induced activation of the ErbB2/ErbB3 signaling through PTPN13 and the phorbol ester-induced disassembly of hemidesmosomes [17]. The gene discussed is CADM4; the disease is neoplasm.