Consistently, we previously found that deletion of Zdhhc9 can reduce the in vivo level of palmitoylated Ras proteins and delay the onset of Nras‐driven leukemia in mice; however, it ultimately fails to prevent disease progress and subsequent mortality.[26] This is partially due to the redundancy within the PAT subfamily, wherein at least three ZDHHC9 PAT homologs, including ZDHHC14 and ZDHHC18, have alternative specificity to catalyze the palmitoylation of NRAS or HRAS.[27]. The gene discussed is NRAS; the disease is leukemia.