JUN and neoplasm: Comparison of baseline tumor samples from the two patient cohorts with the most variable responses to NAT revealed a significant downregulation of genes in pCR patients involved the humoral immune response (such as S100A8, IGHG4, S100A9, IGKC, IGLC3, IGHG3, RGCC, HLA-A, IGHG1, CXCL8, CXCL1, A2M, KRT6A, IGHA1, and CXCL2), B cell activation (such as IGHG4, IGKC, IGLC3, IGHG3, IGHG1, BATF, TNFRSF4, RASGRP1, IGHA1, NDFIP1, ZFP36L1, TBC1D10C, andCTLA4), and myeloid cell differentiation (such as JUN, HSPA1B, HSPA1A, JUNB, ZFP36, ADAR, PIP4K2A, NFKBIA, NR4A3, FOS, and GNAS) (Fig. 5B).