Interestingly, reconstitution of CIC repressor activity via ectopic expression of CICS173A, a mutant CIC protein that is less responsive to ERK-mediated inactivation, and ATXN1L, a corepressor required for CIC stability and DNA binding (Lee et al, 2011; Wong et al, 2019), not only reduced tumor cell proliferation, but also restored sensitivity to trametinib. Here, ATXN1L is linked to neoplasm.