Activating mutation of the PIK3CA gene is a common trait in CRC tumors, leading to aberrant activation of the PI3K/Akt pathway2, however, silmitasertib triggered the same G2/M arrest in SW-480 cells (Supp Fig. 2) which, unlike DLD-1, does not contain activating mutations in PIK3CA. These results suggest an effect of the CK2 inhibitor silmitasertib on decreasing tumorigenicity of CRC cells through a G2/M arrest. The gene discussed is AKT1; the disease is colorectal carcinoma.