The potential existence of predisposition circuitries is highlighted by two findings: firstly by the network of genetic interactions of genes shared between cancer samples (P17, P61) and controls (P39, P26, and P84) where the gene ELAVL1/HuR was central together with candidate cancer genes like WHSC1, ERBB2, PRNP, PABPC1, TNFRSF14, MAP2K3, and UBC; and secondly the evolving complexity of interaction networks from control to tumor samples (Supplementary Data: Image 8) which is consistent with the preliminary assumptions we made on a stepwise pattern of predisposition and ordered mutations. This evidence concerns the gene MAP2K3 and cancer.