By contrast, a high frequency of somatic mutations was detected in TP‐53, APC, and K‐ras, etc., which was in agreement with published literature.4 These findings suggest that genetic alterations in T‐synthase, Cosmc and/or C3GnT are not prevailing mechanisms for such a high incidence of aberrant O‐glycosylation in CRC tissues. The gene discussed is APC; the disease is colorectal carcinoma.