Notably, Janakiraman and collogues comparing PDX and the subsequent PDO from pre-neoadjuvant therapy rectal cancer [54] has evidenced a substantial overlap in their mutational profiles (> 80% congruent), identifying APC and TP53 mutations in 83 and 78% of tumors, respectively and loss of heterozygosity of TP53 gene that leads to inactivation of the tumor suppressor genes, stabilizing TP53 mutation and promoting oncogenic gain of function activity [68–70] in 100% of tumors. The gene discussed is TP53; the disease is rectal cancer.