IGF1 and benign prostatic hyperplasia: In addition, the results of KEGG analysis suggested that the most significant pathway was small molecules, which had been shown in previous studies to influence the cell cycle, apoptosis and proliferation [70–72], whereas the upregulated DEGs were most significantly enriched in pathways associated with IGFs and IGFBPs, which have been previously shown to be associated with BPH [28, 73], and inhibition of IGF-1 secretion inhibited the proliferation of prostate epithelial cells [29].