In addition, the probable convergence of ATAD2 on SRC-3 might explain why the inhibitor of ATAD2, BAY850, possessed a relatively low additive cancer cell killing effect in combination with SI-12 across seven out of eight tested cell lines with maximal gap of 30% between the killing effects of a single drug and the combo (Fig. 4b). The gene discussed is ATAD2; the disease is cancer.