REST and cancer: Loss of REST activity mediated by a splicing regulator serine/arginine repetitive matrix 4 (SRRM4) has been suggested to promote the emergence of the NE phenotype in CRPC [111] and endows cancer cells with stemness and neuroendocrine features most likely by de-repressing expression of REST targets such as CD44, Twist1, and secretagogin (SCGN) [131,132].