BCHE and cancer: Of the gene products that are downregulated in this list, OPRK1 likely controls neuroendocrine differentiation [74], NOV suppresses androgen-independent PC growth [71], CAMK2N1 suppresses growth factor-induced PI3K and MEK/ERK proliferative signaling in PC cell lines [64], STAC likely modulates proliferative signaling through its SH3 and cysteine-rich domains, butyrylcholinesterase (BCHE) likely suppresses cholinergic stimulation of PC proliferation [68], and loss-of-function mutations in sucrase-isomaltase (SI) have been associated with cancer-promoting metabolic reprogramming [103].