The disrupters of the hTS dimer administered to OC and CRC cell lines in this work have previously been shown to inhibit enzymatic activity and markedly trigger its proteasomal degradation, resulting in cancer cell growth inhibition both in cultured cells and in mouse models and, unlike traditional hTS inhibitors, not accompanied by over-expression of this critical enzyme for DNA synthesis and thus by the consequent resistance to further treatments (Costantino et al., 2022). The gene discussed is APCDD1; the disease is cancer.