Importantly, Zhang et al. demonstrated that the expression of PI3Kα was negatively correlated with the activity of SAF-248 and found multiple oncogenic pathways, such as IL2_STAT5 (Interleukin-2/Signal Transducer and Activator of Transcription 5), IL6_STAT3 (Interleukin-6/Signal Transducer and Activator of Transcription 3), MTORC1 (Mammalian Target Of Rapamycin Complex 1) and MYC, upregulated in tumor tissues upon prolonged treatment with SAF-248 compared to those with short-term administration, possibly pinpointing to an adaptive mechanism of resistance[83]. The gene discussed is MYC; the disease is neoplasm.