Over the course of past few years, cancer immunotherapy has been accompanied with promising results. However, preliminary investigations with respect to immunotherapy concentrated mostly on targeting the immune checkpoints, nowadays, emerge as the most efficient strategy to raise beneficial antitumor immune responses. Programmed cell death protein 1 (PD‐1) plays an important role in subsiding immune responses and promoting self‐tolerance through suppressing the activity of T cells and promoting differentiation of regulatory T cells. PD‐1 is considered as an immune checkpoint and protects against autoimmune responses through both induction of apoptosis in antigen‐specific T cells and inhibiting apoptosis in regulatory T cells. Several clinical trials exerting PD‐1 monoclonal antibodies as well as other immune‐checkpoint blockades have had prosperous outcomes and opened new horizons in tumor immunotherapy. Nonetheless, a bulk of patients have failed to respond to these newly emerging immune‐based approach and the survival rate was not satisfying. Additional strategies, especially combination therapies, has been initiated and been further promising. Attempts to identify novel and well‐suited predictive biomarkers are also sensed. In this review, the promotion of cancer immunotherapy targeting PD‐1 immunoinhibitory pathway is discussed.

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This review provides an update on the recent gene therapies for DMD that aim to compensate for dystrophin deficiency and the related clinical trials.

Congenital short bowel syndrome (CSBS) is a rare congenital neonatal disorder. CSBS results from intestinal impairment during embryogenesis. Mutated CXADR-like membrane protein (CLMP) and Filamin A genes are involved in the cause of CSBS. In this study, due to our misdiagnosis, we had to perform whole exome sequencing on the patient, and also we implemented cosegregation analysis on his parents with consanguineous marriage and also parents' mothers. We identified a homozygous loss of function mutation in the CLMP gene in exon 5 (c.664C > T, p.R222X). Also, both parents and grandmothers of the proband were heterozygous for this mutation. Loss of function mutation in CLMP causes CSBS, leading to impaired intestinal development.