One area of focus is common fusion of RARα, which occurs in more than 98% of patients,        5  but there are six alternative fusion genes with different chromosomal translocations, which have been observed in rare cases and often lead to resistance to the most common therapies. 6,7  Based on the research cited above, the molecular and genetic mechanisms involved in APL pathogenesis and drug responses remain largely unknown. This evidence concerns the gene RARA and acute promyelocytic leukemia.