In line with these findings, a recent study in multiple myeloma revealed that hyper-acetylation of GLI1 through pharmacological inhibition of class I and II HDACs leads to reduced tumor survival by decreasing nuclear accumulation and transcriptional activity of GLI1, and accelerating its proteasomal degradation (Geng et al., 2018). The gene discussed is GLI1; the disease is AL amyloidosis.