INS and SHORT syndrome: In order to assess the effect of the p85α truncation mutation in a canonically insulin-responsive cell type, lentiviral constructs were used to generate 3T3-L1 murine preadipocytes showing doxycycline-inducible overexpression of WT p85α or one of two p85α mutants — the p.Tyr657X mutation studied in primary cells and the p.Arg649Trp mutation, which accounts for around 50% of SHORT syndrome (Figure 4A).