Targeting ARID1B in ARID1A‐mutated cells increases their sensitivity to infrared radiation (IR); ARID1B knockdown selectively increases the radiation sensitivity of ARID1A‐mutated colorectal cancer (CRC) cells, which is related to the suppression of RAD51 focus formation, and is not dependent on the antiproliferative effect, suggesting that ARID1B may be a potential therapeutic target to enhance the radiotherapy sensitivity of ARID1A‐deficient tumours, and its function in DNA repair still requires further investigation [45]. The gene discussed is RAD51; the disease is colorectal carcinoma.