Important limitations of this study are the lack of examination of the efficacy of DR‐3 and FDR2 in mouse or human models of MASH, which adds the complication of the impacts of steatosis, and an absence of side‐by‐side comparisons of the specificity, potency, and anti‐fibrogenic activities of DR‐3 and FDR2 with other HDAC6 inhibitors such as TYA‐018. The gene discussed is HDAC6; the disease is metabolic dysfunction-associated steatohepatitis.