These alterations are highly correlated with changes in gene expression upon loss of one or both ARID proteins and we observe significant changes in the expression of genes encoding signaling intermediates in cell growth and adhesion, including MET. Applying similar techniques in a naturally occurring ARID1A-mutant ovarian cancer cell line, we find that knockdown of ARID1B results in loss of accessibility and active histone marks around AP-1 motifs at enhancers, suggesting a common mechanistic function for ARID proteins across cancer types. The gene discussed is ARID1B; the disease is cancer.