IL1A and neoplasm: Tumour released IL-1 cross-talks to TAMs and induces M2 polarization to an immunosuppressive phenotype via IL-1 receptor (IL-1R) and myeloid differentiation primary response gene 88 (MyD88), which requires I-kappaB kinase beta (IKKβ)-mediated nuclear factor kappa B (NF-κB) [31, 32].