Other plausible genes implicated in the pathogenesis of PBS include variants in CHRM3 (the muscarinic cholinergic receptor M3 responsible for bladder smooth muscle contraction), ACTA2 and ACTG2 (two actin genes expressed in smooth muscle), HNF1β (the embryonic transcription factor hepatocyte nuclear factor 1β) and STIM1 (the stromal interaction molecule 1 which has calcium channel regulatory activity). This evidence concerns the gene ACTG2 and prune belly syndrome.