In addition to that, our study showed that unlike AML [80], melanoma [18, 81], and multiple myeloma [82], where LILRB4 has been shown to support tumor progression by activating STAT3 and inhibiting NF-κB, our study uncovered a new LILRB4 signaling mechanism that regulates CRD-induced mammary tumorigenesis via a noncanonical WNT signaling pathway via activation of JNK, c-FOS, c-MAF and the downstream target ARG1. The gene discussed is NFKB1; the disease is acute myeloid leukemia.