Non‐cardiovascular toxicity was also similar in both the R‐CHOP and R‐COMP groups, in contrast to some of the findings reported by Fridrik et al.23In fact, whereas in the study by the Austrian group the number of SAEs was higher in R‐CHOP compared to R‐COMP patients (40 vs. 26, p = 0.029) due to increased infections, this was not the case in our study, with more SAEs being observed in the R‐COMP group because of febrile neutropenia, bleeding and pyrexia episodes, and despite a trend to higher incidence of neutropenia in R‐CHOP patients. The gene discussed is DDIT3; the disease is neutropenia.