Subsequent studies by this same group extended these findings to show that the repressive chromatin landscape of EGFR-mutant NSCLC persisters results from histone modifications orchestrated by the action of multiple histone methyltransferases and HDACs including SETDB1, G9a, EZH2, HP1, ATRX, and class I HDACs [24]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.