When ARID1B is knocked down, a selective increase in the radiation sensitivity of ARID1A mutant CRC cells is witnessed, which is associated with the suppression of RAD51 focus formation and the impairment of Homologous Recombination, suggesting that ARID1B may potentially serve as a therapeutic target for enhancing the radiation sensitivity of ARID1A‐deficient tumours [45]. The gene discussed is ARID1A; the disease is neoplasm.