Methylation of the TSS1500 of IGFBP5, which encodes an endogenous IGF1R inhibitor and is expressed at low levels in the POU2F3-regulated tuft cell-like SCLC subtype and at high levels in the subtype with high ASCL1 expression [12, 13], was associated with resistance to the mTOR inhibitor INK-128 (sapanisertib; ρ = 0.5107, pFDR = 0.0896; Table 4). This evidence concerns the gene ASCL1 and small cell lung carcinoma.