This dual functionality suggests that CTSD could play a significant role in the progression of AML by influencing cell fate decisions, thereby contributing to the disease’s aggressive nature.[16] Although no statistically significant differences in CTSD expression were found among AML FAB subtypes, expression levels were consistently higher than in controls, indicating CTSD may serve as a broad-spectrum diagnostic marker for AML, independent of morphological classification. The gene discussed is FANCB; the disease is acute myeloid leukemia.