Hypoxia suppresses the M1 macrophage anti-tumor pro-inflammatory phenotype [229–233] by promoting cytoplasmic stress granule sequestration of splicing factors, including CELF1, helping to explain why M1 macrophages express hundreds of spliced RNAs not expressed by M2 tumour-promoting TAMs, implicating hypoxia-induced cytoplasmic CLEF-1 retention in promoting the alternative splicing events that promote and maintain the M2 macrophage tumour promoting phenotype [234]. Here, CELF1 is linked to neoplasm.