In addition, DTYMK could competitively combine with miR-378a-3p to maintain the expression of MAPKAPK2 and thus activate the phospho-HSP27/NF-κB axis, which mediated drug resistance, proliferation of tumor cells, and infiltration of CD163+ M2-type TAMs by inducing the expression of CCL5. This evidence concerns the gene NFKB1 and neoplasm.