An understanding of the molecular basis of both diseases has resulted in the development of more targeted biologic therapies. The diversity of atopic and psoriasis eczema is reflected by the responses to these targeted biologic agents. Hence, blocking a Th1-mediated and Th17-mediated immune disease with a specifically targeted agent may create a flare of Th2-mediated disease.8,15 However, since Th2 cytokines are overproduced by the cellular infiltrate of atopic eczema lesions, interleukin-4 would not be likely to ameliorate skin symptoms of atopic eczema. In fact, biologic drugs particularly inhibiting one T-cell subset seem to be ineffective for the treating co-happening psoriasis and atopic eczema. Ustekinumab is effective in treating psoriasis,18 whereas evidence-based data concerning its influence on atopic eczema are lacking.Although the TSC2, TP53, and FLCN alterations were approximated to be there in 98 to 100 percent of the tumor cells in both pretreatment and resistant tumors, the approximated proportion of malignancy cells with MTOR F2108L was 0 percent in the pretreatment tumor as compared with 96 percent in the resistant tumor . To your knowledge, MTOR mutations have not previously been determined in sufferers with acquired level of resistance to everolimus, and this particular mutation has not been described in patients.17 Resistance to Allosteric mTOR Inhibitors Resulting from mTORF2108l Although MTOR F2108L has not been described previously, the homologous mutation was characterized 20 years ago in fission yeast almost.18 In a mutagenesis screen to identify mutations in tor2 that conferred resistance to rapamycin, tor2 F2049L was one of five rapamycin-resistant mutants identified.