A number of different pathways altered in liver cancer converge towards the activation of the myc oncogene. Our MuPrime™ liver cancer tumor homograft models are transplant of GEMM liver tumors, developed by conditional overexpression of c-Myc (H11-LSL-Myc mouse), into syngeneic hosts. Our tumor homografts preserve the original GEMM tumor driver mutations and provide robust and synchronous growth for in vivo pharmacology studies.