Although it may be tempting to speculate that ALLINI treatment imparts aberrant IN hyper-multimerization in the absence of LEDGF/p75 and HDGFL2 during the early phase of HIV-1 infection, binding to nucleic acid shields IN from the ALLINI-induced effect [50,82], indicating this may not be at play in DKO cells, which support normal levels of reverse transcription [44]. The gene discussed is HDGFL2; the disease is HIV-1 infection.